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Chronic General Periodontitis 

" Periodontal Disease " (Pyorrhoea Alveolaris) 


J. F. COLYER, F.R.C.S., L.R.C.P., L.D.S. 

Denial Surgeon to the Charing Cross Hospital and the 

Royal Dental Hospital of London ; 

Examiner in Dental Surgery Royal College of Surgeons of England 













The following pages treat of the morbid condition of the 
teeth which is characterized by a slowly progressive destruction 
of the tooth attachments. The condition has been variously 
designated, but the term pyorrhcea alveolaris has probably been 
most commonly used and no doubt at one time appeared to be 
justified by what were considered to be the clinical characteristics 
of the condition. Recent investigations have added to our 
knowledge of the causes and development of this condition, and 
what was regarded as a specific disease by earlier writers is to-day 
recognized as a suppurative stage of a disease which can now 
be traced through all its stages from its early beginning as a 
marginal gingivitis to an advanced suppurative condition of the 

The outstanding feature of the disease is a chronic infection 
of the periodontal membrane, and it would seem to be more 
appropriate therefore to describe the disease as a chronic general 

The disease has attracted my attention for many years and, 
from time to time, I have published papers dealing with its 
various aspects. This book is to a great extent a reprint of those 
papers and it is being published in the hope that it may be 
helpful to those who day by day are endeavouring to grapple 
with this widespread disease. 

I desire to take this opportunity of expressing my appreciation 
of the valuable assistance rendered by several friends in the 
preparation of this book, and I wish particularly to record my 
obligations to Mi'. W. Lang, who kindly wrote the section on eye 
lesions and dental sepsis; to Mr. Penfold for his investigation 
into the relation of the Entamoeba buccalis to the disease; to Mr. 
J. Eyre for revising the section dealing with vaccines ; to my 


colleague, Mr. Norman Bennett, for the section on ionic treat- 
ment, and to Mr. H. Darby for much kind help. 

For the loan of blocks for the illustrations I wish to express 
my thanks to Messrs. Longmans, Green and Co., The Royal 
Society of Medicine, and the Medical Committee of the Royal 
Dental Hospital. 

f. F. COLYER. 

May, 1916. 




The Macroscopical Anatomy of Chronic General Perio- 
dontitis ... ... ... ... ... ... ... i 


The Microscopical Anatomy of Periodontal Disease ... 31 

The Clinical Appearance of Periodontal Disease ... ... 38 

The Pathology of Periodontal Disease ... ... ... 46 

The Etiology of Periodontal Disease ... ... ... 62 


Periodontal Disease as the Active Agent in the Production 

of Pathological Lesions ... ... ... ... .. 64 

The Treatment of Periodontal Disease ... ... ... 77 

Chronic General Periodontitis 

(Periodontal Disease, Pyorrhoea Alveolaris). 


The Macroscopical Anatomy of Chronic General 

Before a description is given of the morbid anatomy of 
periodontal disease, it is necessary to consider certain aspects 
of the normal anatomy of the parts involved in the disease, 
in order that the pathological changes may be more readily 

Fig. i shows the mandible of a female, aged 22. The 
alveolar process may be regarded as normal. The alveolar 
process and the teeth sockets are everywhere lined with a fairly 
dense layer of bone, which appears in the skiagram (fig. 2) as 
a dark line. On the buccal aspect in the premolar and molar 
region the margin of the bone is close below the necks of the 
teeth, and, stretching across from one tooth to another in a 
straight line, forms the base of a definite triangular space 
between the approximal aspects of the teeth. In the incisor 
region the bone does not follow a straight line, but is 
continued upwards, so that the space between the incisors is 
considerably less than between the premolars and molars. The 
margin of the bone presents a regular outline, and the surface 
of the bone, which is smooth, is pierced here and there with 
nutrient canals. The appearance of the bone in skiagrams is 
shown in fig. 2. Between the front teeth the bone has the 
appearance of a sharp spine, but it passes in a straight line 
between the back teeth. The outer aspect of the bone shows a 



dense layer, the inner part presenting a cancellous appearance. 
In the maxilla a similar condition obtains. 1 

As age advances there is a gradual tendency for the alveolar 
process to disappear. In healthy mouths, the gum margin re- 
cedes as the alveolar process disappears and a layer of compact 

Fig. I. — Mandible of female, aged 22, with an alveolar process which may 
be regarded as noimal. 

Fig. 2.— Skiagrams showing the appearance of the bone in the mandible (fig. 1). 

tissue is constantly present over the alveolar process. The 
skiagrams of an individual aged 30 with normal gums are shown 
in fig. 3. The muco-periosteum should be firm and pale pink in 
colour. It should blend with the periodontal membrane at the 

1 The skiagram of the incisors shows a slight break in the compact 
tissue towards the apex of the spine, but this is due to slight fracture {post 


neck of the tooth, the junction being distinguishable by the greater 
density in the character of the fibrous tissue. The gingival 
margin of the muco-periosteum is not attached to the tooth on 

Fig. 3. — Skiagrams of alveolar process of an individual with normal gum. 

Fig. 4. - Maxilla which shows slight destruction of the bone in the centre of 
the interproximal spaces. 

the general level of the gum, as the gum falls slightly before 
reaching the tooth and forms a slight depression around the 
tooth. This depression is generally termed the " gingival space," 
but the term " space " is not altogether satisfactory as the soft 


tissues actually lie in contact with the surface of the tooth. 
The floor of the depression is at the neck of the tooth, and 
consequently with the eruption of the tooth the depth of the 
depression decreases. The physiology of the " gingival space " is 
not known. 

Clinical experience shows that periodontal disease usually 
originates in the molar region or around the incisors. When 

Fig. 5. — Skiagrams of maxilla shown in fig. 4. 

Note that the destruction of the bone has already commenced in the 
interproximal spaces. 

FlG. 6. — Maxilla in which the destruction of the bone has advanced beyond 
the stage shown in fig. 4. 

it originates around the back teeth the initial lesion in the bone 
is a slight destruction of tissue in the centre of the interproximal 
spaces as shown in fig. 4, a specimen which has the appearance 
of being normal unless carefully scrutinized. In the next 
specimen (fig. 6), the disappearance of the layer of dense tissue 
and the breach into the cancellous bone indicate that the 
destruction of the bone has already commenced. 


As the destruction of the bone proceeds the outer and 
inner plates of the alveolar process become involved, but the 
loss of tissue, as a rule, is greater between the teeth than on the 
buccal and palatal aspects. This stage is shown in fig. 6. 

Fig. 7. — Maxilla showing considerable destruction of the alveolar process. 

Fig. 8. — Specimen in which the disease probably commenced around the incisors. 

It will be observed that : — 

(1) The destruction of bone around the front teeth is 
considerably less than around the premolars and molars ; and 
(2) the loss of tissue around the molars is greater than around 
the premolars. 

A further stage of the disease is shown in fig. j. The bone 
has so far disappeared as to expose about half of the roots of 


the incisors unci two-thirds of the roots of the molars. Around 

the canine and premolars the bone destruction is less advanced. 

A specimen in which the disease probably commenced 

around the incisor teeth is shown in fig. 8. There is some 

Fig. 9. — Skiagrams of specimen shown in fig. 8. The extent of the bone lesion and 
the resistance of the tissue between the central incisors is clearly shown. 

Fig. 10.— This specimen from a male, aged 30, shows the moibid anatomy of 
an advanced case of periodontal disease. 

loss of bone between the teeth, and the roots on the labial 
aspects are uncovered. The margin of the bone shows the 
pitted, irregular appearance characteristic of rarefying osteitis. 
It will be observed that there lias been less destruction of bone 
between the central incisors than between the other front teeth. 


An examination of the specimen shows that around the 
incisors the destruction of bone is more advanced than around 
the molar teeth. The skiagrams (fig. 9) bring out clearly the 
extent of the bone lesion and also the resistance of the tissue 
between the central incisors. 

The specimen shown in fig. 10 from a male, aged 30, is an 
excellent example of the morbid anatomy of an advanced case. 
The bone around the incisors has almost disappeared, and the 

Fiu. n. — Skiagrams of maxillx shown in fig. 10. 

molar teeth are uncovered nearly to their apices. Around the 
teeth are cup-shaped spaces which are due to the fact that the 
bone bordering the tooth disappears first. The appearance of 
the bone shows that there has been a marked rarefying osteitis. 
Nodular deposits of calculus are present on the teeth, and it 
will be observed that these are, in the case of the incisors, 
canines, and premolars, well away from the margin of the bone. 
The skiagrams of this specimen are shown in fig. n. The 


cup-shaped absorption of the socket is clearly shown in the right 
first molar of the specimen illustrated in fig. 12. Around the 
second molar the destruction of the bone has been of a more 
chronic type, the cup-shaped absorption being absent. The 

Fig. 12. — Maxilla showing cup-shaped absorption of the bone around the 
right first molar. 

Fig. 13. — Skiagram 01 the first and second molars in fig. 12, showing the different 
degrees of bone destruction around these teeth. 

skiagram of these teeth (fig. 13) shows a very distinct difference 
in appearance. Around the roots of the first molar there is a 
definite clear area and the dense layer which marks the outline 
of the normal socket is absent. The bone around the tooth 
shows definite signs of rarefying osteitis. The bone bordering 


the roots of the second molar still retains the dense appearance 
and this indicates that the rarefying process has not spread deep 
into the bone around the tooth. 

In the final stage of the disease the teeth fall out owing to 
the extent of bone destruction. The specimen shown in fig. 14 
is an excellent example. The premolars and molars have fallen 
out and the alveolar process has entirely disappeared. The 
condition of the mandibular canine shows how the final loss 
of the tooth is brought about. In the living subject this 
advanced stage of the disease is denoted by the absence of 
" ridges." 

Fig. 14. — Final stage of the disease. The teeth have fallen out owing to the 
extensive destruction of the surrounding bone. 

In specimens showing marked attrition of the teeth the outer 
aspect of the alveolar process is often thickened and the rarefac- 
tion of the bone is limited to the alveolar margins. A case of 
this type is shown in fig. 15. The skiagrams (fig. 16) show that 
the -rarefying process is almost entirely limited to the surface, 
and has not spread deeply into the sockets. Compare the 
skiagraph appearance of the bone around the incisors in this 
specimen and in the specimen shown in fig. 10. The marked 
attrition of the teeth indicates that the function of mastication 
has been efficiently performed, and the bone around the teeth 




having therefore been kept well nourished with a plentiful flow 
of blood was in a favourable condition to react to injury. 

A specimen in which there is greater thickening of the bone 
is shown in fig. 17. The position of the calculus in relation to 

Fig. 15. — A specimen in which the bone shows marked reaction. Note the 
thickened margin of the alveolar process. 

Fig. 16. — These skiagrams of fig. 15 show that the rarefaction of bone is to a great 
extent limited to the surface. 

the margin of the bone is evidence that well-defined pockets- 
existed around the teeth. The surface of the bone around the 
tooth shows signs of a rarefying osteitis, but there is no cup-like 


absorption of the bone. The thickened bone beyond the surface 
indicates a " sclerosing" inflammation. The arch is well formed 
and the attrition of the teeth on the masticating surface points 
to good functional activity. 

An example of the formation of nodular masses of bone is 
shown in fig. 18. 

In practice a type of case is met with in which the bone 
destruction on the labial and palatal aspects of the teeth is much 
more advanced than on the approximal aspect. In many of 

Fig. 17. — A specimen from a very chronic case showing considerable thickening of the 

margin of the bone. 

these cases the gum margin is very little above the neck of the 
tooth, and a probe inserted between the gum and tooth will pass 
almost to the end of the root. This condition is generally 
associated with the anterior teeth, and not infrequently with 
patients whose teeth are unduly prominent. A specimen illus- 
trating the morbid anatomy of this type of case is shown in 
fig. 19. The bone on the labial aspects of the right canine and 
central incisor has completely disappeared ; the left central 
incisor and canine are only covered by bone in the neighbour- 
hood of the apex. Note the deposit of calculus around the necks 
of the teeth and the freedom from calculus of the remaining 
exposed portion of the roots. On examining the position of the 



teeth in relation to the bone, it will be seen that the arch is 
decidedly narrow and that the general direction of the teeth is 
too vertical. 

Fig. 18. — A specimen showing the formation of nodular masses on the outside 
of the alveolar process. 

Fig. 19. — In this specimen the bone destruction is most marked on the anterior aspects 

of the teeth. 

A point worthy of attention is that the disease spreads in the 
maxilla more actively and extensively than in the mandible ; 
especially is this the case in the region of the molars. The 



more limited area of bone destruction in the mandible is due 
to the nature of the osseous tissues, the bone in the maxilla 
being of a much more cancellous character than in the mandible. 

Fig. 20 — Mandible from an advanced case of periodontal disease in the region of 
the mandibular molars. 

fThe right 
! premolars 

land molars. 

(The left 
- premolars 
(and molars. 

Tig. 21. — Skiagrams of the specimen shown in fig. 20. 

This difference in the spread of the disease in bones of unequal 
density is more fully dealt w 
disease in the lower animals. 

density is more fully dealt with in the chapter treating of the 

J 4 


A mandible showing extensive destruction of the bone in the 
region of the molars is shown in fig. 20, and the skiagram of the 
specimen in fig. 21. 

The series of specimens just described indicates that the 
bone lesion is a progressive rarefying osteitis which commences 
at the margin of the tooth socket and eventually destroys the 
bone until the tooth is shed owing to the loss of its attachments. 

Fig. 22. — Teeth from a case associated with multiple arthritis. 

Fig. 23. — Teeth from an advanced case which had been treated 
for two years with vaccines. 

The Teeth. 

The teeth from cases of periodontal disease exhibit definite 
changes. The hard tissue shows absorption, and the periodontal 
membrane is thickened — indications of a chronic inflammatory 
process. Teeth removed from a series of cases are shown in 
figs. 22, 23 and 24. Those depicted in fig. 22 were taken from a 
man, aged about 34, who was a mouth-breather and was suffering 
from mucous colitis. A year previously he had had an attack 
of arthritis involving several of the large joints. 

When the hard tissues around the apex of a tooth are being 
absorbed the presence of periodontitis is indicated, and peri- 
odontitis necessarily implies pathological changes in the adjacent 
bony tissue. The degree of rarefying osteitis may be gauged 


by the rapidity of tooth absorption and the liability to direct 
infection of the tissues increases in proportion to the amount of 
rarefying osteitis. The condition of the teeth in fig. 22 indicates 
that there was marked rarefying osteitis and probably direct 
absorption of toxins, &c, into the blood-stream. 

Large masses of adventitious tissue are frequently found 
in the cleft between the roots of the molar teeth, indicating 
extensive loss of osseous tissue at those points. The condition 
of the teeth in cases exhibiting deep pockets and profuse 
suppuration is well shown in the specimen illustrated in fig. 23. 

Fig. 24. — Teeth showing changes at their apices. 

In many cases of periodontal disease the teeth become very 
brittle. There is some doubt as to the real cause of this brittle- 
ness. Mr. J. G. Turner attributes it to malnutrition of the 
dentine caused by toxins absorbed via the cementum. My own 
view is that the fragility is due to increased calcification of the 
soft parts of the dentine and cementum, and that the process is 
as follows : The toxins injure the tooth tissues, which, like other 
tissues of the body, react, the reaction taking the form of an 
increased calcification of the soft contents of the dentinal tubes 
and cemental lacunar, thus causing greater fragility of the tooth, 
and rendering the tooth more brittle. 

I have arrived at this conclusion after staining in borax 
carmine a series of teeth from cases of periodontal disease and 
a careful examination of the teeth themselves. On being held 



to the light such teeth appear more translucent than normal 
teeth, especially about the apices, and if the teeth are immersed 
for six or eight weeks in borax carmine it will be found that the 
translucent area does not stain to the same extent as the other 
parts of the teeth, which indicates that the soft tissue normally 
present has undergone calcification. 

Sections of teeth from three cases of periodontal disease are 
shown in figs. 25 to 27. 

Fig. 25. Fig. 26. 

Teelh from cases of periodontal disease showing translucent areas. 

Fig. 27. —Teeth from a case of periodontal disease showing translucent areas. 

Periodontal Disease in Animals. 

Periodontal disease frequently occurs in horses, in cats and 
dogs and captive wild animals, and it is more rarely met with 
in animals in the wild state. A study of the disease in these 
animals is very instructive, and throws much light on the etiology 
and pathology of this serious affection. It will be convenient to 
consider this section under two headings : (a) wild animals and 
(b) domestic animals. 



(a) Wild Animals. 

The Odontological Section in the Museum of the Royal 
College of Surgeons of England contains a unique collection 
of skulls, showing the disease in a wide range of animals, 
including rodents, marsupials, herbivora, monkeys, edentata, and 
the small and large carnivora. 

FlG. 28. — Macropus bennetti (Bennett's wallaby), showing an early stage of peiiodontal 
disease. The loss of bone is more marked in the maxilla than in the mandible. 

Fig. 29. — retiogale penicellala (brush-tailed kangaroo). In ihis specimen the 
disease is more advanced than in specimen fig. 28. 

Four specimens in this collection showing various stages of 
the disease in the kangaroo will be considered first. 

(1) A Bennett's wallaby (Macropus bennetti, fig. 28) exhibits 
an early stage" of the disease; the septa between the anterior 



teeth of the maxilla have been partially destroyed, while in 
the region of the maxillary first molars the bone shows signs 
of rarefying osteitis. 

(2) The skull of a brush-tailed kangaroo (Petrogale penicellata, 
fig. 29) shows a further stage, the disease being more generally 
distributed and the mandibular teeth more affected than in 
specimen fig. 28; a slight deposit of calculus is seen on the teeth. 

Fig. 30. — Macropus. Species unnamed. In this specimen the disease is well 
advanced, more especially in the region of the maxillary molars. 

Fig. 31. — Macropus. Species unnamed. The majority of the teeth have been 
lost from the disease. 

(3) In the skull of a macropus (species unnamed, fig. 30) the 
disease is still further advanced, the bone being extensively 
destroyed in the neighbourhood of the right maxillary third 
molar; signs of rarefying osteitis are plentiful, while in the 


mandible there is distinct thickening of the bone around the 
right first molar. 

(4) In the left half of the skull and mandible of a kangaroo 
all the molars have been lost except one in the maxilla and one 
in the mandible, and around these teeth the bone has been 
extensively destroyed (fig. 31). 

In the carnivora a similar gradational series can be traced, 
the point of special interest being that the disease tends to spread 
in the maxilla more rapidly than in the mandible, owing probably 
to the former bone being less dense in character. This difference 
in the spread of the disease is well shown in the specimen of 
a common wolf (Cam's lupus) depicted in fig. 32. 

Fig. 32. — Cam's lupus (wolf). The disease has spread more in the maxilla 
than in the mandible. 

The bone around the maxillary fourth premolar has almost 
disappeared. The cup-like absorption of the socket can be well 
seen and the large area of rarefying osteitis indicates the spread 
of infection into the bone. In the mandible the disease is not so 
advanced and the outer layer of bone does not show signs of 
rarefying osteitis. 

Among the suricates the mandible is more often affected 
than the maxilla, and this may be due to the shape and arrange- 
ment of the teeth of this animal. The mandibular molars are 
often slightly crowded and the shape of the teeth is such as to 
assist the lodgment of food. The mandible of one of these 
animals is depicted in fig. 33. It will be observed that the 



setting of the premolars and molars is slightly irregular, that 
the alveolar process has been extensively destroyed, especially 
in the region of the molars, and that the bone absorption is greater 
between the teeth than on the buccal and lingual aspects. 

FlG. 33. — Swicata teliadactyla (suricate). Mamlible showing the slightly irregular 
arrangement of the molars and premolars. 

FlG. 34. — Cervs ddii (Panolia deer). The destruction of the bone is most 
marked in the region of the first molars. 

In the herbivora the disease is common ; but rarefying 
osteitis of the outer alveolar plate is comparatively rare, and this 
is a point of special significance in view of the fact that, as 
compared with the carnivore, the bone of the maxilla in the 
herbivora is more dense and there is a smaller proportion of 


cancellous bone. It seems probable, therefore, that the rapidity 
in the spread of the disease is to some extent governed by the 
density of the bone. A specimen illustrating the resistance of 
the bone in the herbivora is seen in the skull of a Panolia deer, 
Cervus chiii, shown in fig. 34. 

Another point of interest in this skull is that the destruction 
of tissue is greatest in the region which bears the main force of 
mastication. In the recent state the spaces formed between the 
teeth are choked up with fodder. 

A more advanced stage of the disease is seen in a Schom- 
burgk's deer {Cervus schomburgki) (fig. 35). 

Fig. 35. — Cervus schomburgki (Schomburgk's deer). An advanced stage 
of the disease. 

This specimen serves to emphasize the limitation of the 
infection of the bone in the herbivora. Although the disease 
was present in an aggravated form, the bone was only very 
slightly affected beyond the immediate neighbourhood of the 

In the specimen shown in fig. 36 the infection around the 
mandibular teeth has spread to the body of the bone and has 
resulted in extensive necrosis of the coronoid process. 

This tendency to excessive suppuration in the body of the 
bone may be due to the shape of the teeth in herbivora. 
The teeth are of the hypsodont type, and the infection from 


the pockets around the teeth is carried via the periodontal 
membrane deep into the substance of the bone and spreads 
rapidly in the cancellous tissue, the spread to the coronoid 
process and not to the condyle being again accounted for by 
the former offering a path of least resistance. 

Fig. 36. — Cervus (species unnamed). In this specimen there has been suppuration 
in the body of the mandible from in'ection around the teeth. 

Fig. 37. — Ursus omatus (spectacled bear). The disease in this specimen probably 
followed on injury to the right maxillary canine. 

The theory that the disease may be started by an injury is 
supported by such cases as that shown in fig. 37. The skull is 
that of a spectacled bear {Ursus omatus) from the Andes of Peru. 
This animal was in the Zoological Society's Gardens for nearly 
fourteen years, and at its death the right side of the mouth 


presented the condition shown in fig. 37. The teeth that remain 
are only slightly fixed to the bone and are heavily coated with 
salivary calculus, a large mass being adherent to the buccal 
aspect of the maxillary right molar. The teeth on the left side 
show an early stage of the disease. The interesting feature of 
this specimen is that the pulp of the right maxillary canine had 
died owing to the exposure of the pulp chamber through attrition 
or fracture, and it is highly probable that the trouble to the 
canine accounted for the severity of the disease on the right side 
by creating a tender area, and so interfering with the functional 
activity of the teeth on that side of the mouth. 

Fig. 38. — Cam's familiar-is (pug dog). The disease is limited to the mandibular 
incisors, which are functionless teeth. 

Animals in the wild state are by no means immune to 
pathological changes in the alveolar process, and in a recent 
examination I have made of the collection of skulls of monkeys 
in the British Museum several examples of definite periodontal 
disease were noticed. The feature of interest was that animals 
in certain localities seemed to be especially liable to the disease. 



(6) Domestic Animals. 

Among domestic animals the cat, the dog, and the horse are 
the chief sufferers from periodontal disease. 

From the dogs we are able to obtain some instructive data 
concerning the disease. In the short-muzzled breeds, such as 

Fig. 39. — Canis familiar is (variety unnamed). An advanced stage. The disease ] 
commenced around the mandibular incisors. 

Fig. 40. — Canis familiaris (Maltese terrier). An advanced stage of periodontal 
disease in a "Society pet." 

the pug and the bull-dog, the disease usually starts around the 
mandibular incisors, the maxillary incisors becoming subsequently 
involved (fig. 38). 

Towards the back of the mouth a common starting-point of 
the disease is the region of the second and third premolars. In 


the short-muzzled breeds these teeth are often placed obliquely 
to the line of the arch, and are so crowded as to form excellent 
crevices for the lodgment of food. In the long-muzzled breeds 
the disease usually starts between the premolar and molars, 
a frequent site being the angle formed between the last premolar 
and the first molar on the palatine aspect. From these early 
beginnings the disease can be traced through all stages to the 
final loss of the teeth through complete destruction of the alveolar 
process as shown in figs. 39 and 40. 

— r 

1 H 





Fig. 41. — Equus caball us (horse). A specimen with the muco-periosteum of the 
palate in place. The teeth are carious. The first stage of periodontal disease is shown 
in the slight destruction of the muco-periosteum between the last two molars on the 
right-hand side of the illustration. 

Among the lower animals the horse supplies us with the most 
instructive lessons concerning the disease, since it is possible 
to follow without difficulty every stage from the initial lesion 
to the advanced suppurative condition. 

The following illustrations show the various stages of the 
disease in the horse. 

The earliest stage is shown in fig. 41. This specimen of the 



maxillae of a horse affected with caries has been prepared with 
the muco-periosteum in position. The initial lesions of the 
muco-periosteum are seen between the last two molars on the 
right side of the picture and the second and third premolars on 
the left side. 

Fig. 42. — Equns caballus (horse). An early stage ot the bone destruction. 

Fig. 43. — Eqims caballus (horse). The bone destruction has advanced sufficiently 
to loosen the attachment of the first molar. 

The next stage is shown in tig. 42. The loss of bone on the 
inner aspect of the teeth is well marked, the interproximal spaces 
being most affected. 

A further development is illustrated in fig. 43. The bone 
destruction has progressed to such an extent that the first molar 
is quite loose and is being extruded from its socket. Here, 



as in the preceding specimen, the interproximal spaces are most 

The formation of spaces between the teeth is shown in 
fig- 44> and fig. 45 gives a good idea of the condition of many 

Fig. 44. — Equns caballus (horse). Showing spaces formed between the teeth. 

Fig. $$.—Equus caballus (horse). Shows the spaces filled with fodder. 

of these spaces when seen in the fresh, moist condition. They 
are packed full with fodder and other material. 

The effect of the food packing on the soft tissues is seen 
in fig. 46, which shows a portion of a mandible prepared with 
part of the muco-periosteum in situ. The infection from the 



space between the fourth premolar and the first molar has 
spread to the body of the bone and has led to the formation 
of an abscess. 

Fig. 46. — Equus caballus (horse). Showing the condition of the soft tissues from 

the food packing. 

Fig. 47. — Equus caballtts (horse). From a well-marked case of periodontal disease 
in which there has been suppuration in the body of the bone. 

Another preparation illustrating the infection of the body of 
the bone from the spaces between the teeth is shown in fi<4. 47. 
The spaces are filled with fodder ; there has been suppuration in 
the body of the bone and considerable thickening of the outer 
layer of the bone. 


2 9 

Finally, the specimens in figs. 48 and 49 show the advanced 
stage in an animal which I examined when alive. Pus was 
flowing freely from the mouth, a foetid discharge was flowing 

Fig. 48. — Eqttu scaballus (horse). From an advanced case. A director is placed 
in a sinus leading to the antrum. 

FlG. 49. — Equus caballus (horse). The left maxilla and mandible from the same 
case as shown in fig. 48. 

from the nostrils, and the sulcus between the cheeks and teeth 
was clogged with food. The animal was killed and the head 
prepared partly as a moist specimen and partly as a dry specimen. 


Fig. 48 shows the right maxilla. The premolars and molars are 
carious. The margin of the gum is thickened and detached 
from the bone. Between the second and third molars there is 
a huge space which communicates with the antrum, the lining 
membrane of this cavity being thickened and inflamed. The 
left half of the skull and the mandible (shown in fig. 49) give 
a good idea of the bone lesions. Several of the teeth, both in 
the maxilla and mandible, are carious, the alveolar process has 
been extensively absorbed, the greatest loss of tissue being in the 
region of the two last maxillary molars. The space between 
these teeth communicates with the antrum. The buccal aspects 
of the posterior teeth show signs of caries, which was no doubt 
due to the lodgment of food in the buccal sulcus. Had we not 
been able to observe the disease in the horse through the 
progressive stages shown in figs. 41 to 47 it would have been 
difficult to understand how such an extreme condition as is 
manifest in this case could have been the direct result of a slight 
injury to the muco-periostenm. 

The conclusions to be drawn from an examination of the 
disease in man and other animals are : — 

(1) That the bone lesion is a progressive rarefying osteitis 
commencing at the margin of the alveolar process, and (2) that 
the varying density of the bone influences the rate of destruction. 


The Microscopical Anatomy of Periodontal Disease. 

The knowledge which we possess of the microscopical 
anatomy of periodontal disease is based mainly on the work of 
Znamensky and Talbot. Dr. Znamensky has given us in detail 1 
the results of his examination of sections from the jaws of a 
female, aged 39, who died of acute anaemia resulting from 
haemorrhage after parturition. "The decalcification of the 
preparations was accomplished by means of a 3"5 per cent, 
solution of trichloracetic acid." Some of the sections were 
stained with eosin and hematoxylin and others with Hoeffler's 
blue. The sections show that the earliest pathological changes 
commence at the gum margin and that subsequently the 
periodontal membrane and adjacent bone are successively 
involved. The illustrations given in Dr. Znamensky's paper 
show clearly the different stages of the disease. Fig. 50 shows 
the earliest stage. The epithelial covering of the gum is still 
intact, but in the papillary layer there is an infiltration of the 
tissues with leucocytes. The remaining portion of the gum 
and the bone are normal. 

The next section (fig. 51) depicts a further stage; the 
destruction of the epithelial layer has commenced and the gum 
is infiltrated with leucocytes almost to the edge of the bone. 

Fig. 52, to quote Znamensky, "represents the period of the 
disease when the infiltration has already reached the bone, and 
from this moment the changes in the bone of the socket begin. 
First they appear upon its free rim. " For better evidence 

1 Transactions International Medical Congress, 1913 (Stomatological 



I took that part of the socket where, examined by the naked 
eye, it has the thickness of a sheet of paper, and under the 
microscope appears to be a narrow, long plate not containing 
any bone-marrow. The destructive process is proceeding in it 
in this manner: First the socket loses lime salts, and gets trans- 


- . 

m i 

'A ■■.;. - ; .V V $ 

Fig. 50.' — d, dentine;/, calculus;/, papil- 
lary layer of the gum; 2, epithelial layer; i, 
tissue infiltrated with leucocytes; c, normal 
gum ; y, normal bone. Magnified 80 times. 


Fig. 51. — A more advanced stage than 
that shown in fig. 50. The destruction of 
the epithelium has commenced at // and j'. 
Magnified So times. 

formed into an osteoid tissue, and afterwards into a fibrous con- 
nective tissue. Directly this is done the infiltration with white 
blood corpuscles begins. Those places of the thin socket which 

' The description of the sections are copied from Dr. Znamensky's paper. 

I if t I 

Fig. 52.—?', infiltration proceeding from the gum to the bone ; s, the part next to 
the infiltrated part of the socket is transformed into a fibrous connective tissue ; 0, osteoid 
tissue ; d, part of the bone beginning to lose its lime salts ; «, bone corpuscles ; /, broken 
line dividing the healthy part from the affected bone ; v, alveolar periosteum not yet 
inflamed ; D, dentine. Magnified 180 times. 



Fig. 53. — o, place where the osteoid tissue has had time to be gnawed by inter- 
vening tissue, infiltrated with leucocytes ; /;/, place where the bony plate of the socket 
has had time to be half gnawed by osteoid tissue; i, infiltration of the intervening tissue 
is more sharply expressed ; v, periosteum of the socket beginning to react ; the blood- 
vessels becoming wider at /'. Magnified 180 times. 



began to lose lime, when magnified by the aid of a microscope, 
present a uniform homogeneous semi-lucid mass, in which no 
bony laminae are to be seen ; and the bone corpuscles lessened 
in their number have lost their characteristic forms, and have 
become more and more like the cells of a connective tissue. 
The bone which has been altered in that manner is very 

FlG. 54. — 0, outside of the tooth socket being connected with osteoid tissue ; b, inside 
of the tooth socket showing Howship's lacunrv ; g, osteoclasts ; /, the so-called lacunar 
absorption of the bone is proceeding ; the blood-vessels of the periosteum, k, are dilated, 
but the periosteum is but little infiltrated, the gum, on the contrary, showing considerable 
infiltration ; s, reaching the bone of the socket ; D, dentine. Magnified 180 times. 

distinctly divided with a broken line from the neighbouring 
healthy part of the bone, and by a similar broken line it is 
again divided from that other part of the bone which has 
already had time to change into a fibrous tissue, and the 
peripheral part of this latter passes quite imperceptibly into the 
fibrous connective tissue of the gum. Thus, microscopically 
examined, we see the following : beginning from the free edge, 



Fig. 55. — This section shows the primary alterations in the marrow part of the bone 
of the socket. The absorption of the bone from the side of the periosteum is proceed- 
ing, a ; and from the Haversian canals, b, upon the margins of healthy bone, i.e., the 
part which begins to get decalcified, </, all round the Haversian canal the inner layer of 
the decalcified bone is transformed into an osteoid tissue, 0, and this latter nearer to 
translucent part of the Haversian canal has already passed into a fibrous connective 
tissue, s, impregnated with infiltration, i ; the same order of alterations in bone pro- 
ceeds also from the side of the periosteum of the root ; /' osteoclasts. Magnified 
360 times. 

«t. ri ■< /&>e*~*4*^i.. 

\ Fig. 56. — This section shows the concluding stage of the development of the disease 
in the marrow part of the bone ; bony aminie are absorbed and transformed into fibrous 
connective tissues very strongly impregnated with inflammatory infiltration. There is a 
sequestrum to be seen which is beginning to be absorbed from the periphery. Magni- 
fied 360 times. 



a part of the bone of the socket is already transformed into 
connective tissue, which passes deeper into an osteoid tissue. 
There is a place to be found where the osteoid tissue has already 

K E L M 

(From a drawing by Mr. A. Hooewell-Sniith). 

FlG. 57-' — A, pulp cavity ; B, dentine of tooth ; c, hyperplasic cementuni 
around apex of root : i>, periodontal membrane, greatly thickened — hyperplasic ; 
E, indifferent tissue at apical region greatly increased in amount ; F, free edge of 
bone of socket becoming converted into fibrous intervening tissue ; G, bone of socket 
presenting earliest signs of osteoporosis; h, large osteoporotic space in bone of jaw- 
filled with bone-marrow ; I, bone of socket paitially decalcified and converted into 
osteoid tissue ; .1, junction of living with decalcified bone ; K, osteoclasts producing 
lacunar absorption ; L, bone of jaw only slightly altered by disease; M, sequestrum 
undergoing peripheral absorption ; N, soft, cancellous tissue slightly changed from 
normal ; o, inflammation of gum at neck of tooth. 

had lime, so to speak, to gnaw away the bony plate of the 
socket across its breadth (fig. 53). At this period inflammatory 
reaction can be traced in the periosteum, the blood-vessels 

From the Lancet. 


dilate and the tissues become infiltrated with leucocytes." A 
further stage of the bone destruction is shown in figs. 53 and 54. 

The bone is hist decalcified, then gradually transformed into 
an osteoid tissue and afterwards into a connective fibrous tissue 
which becomes infiltrated with leucocytes. In the deeper parts 
of the tooth socket the tissue changes are in part similar to 
those thus described ; the so-called lacunar absorption of the 
bone is, however, more pronounced, the absorption proceeding 
not only from the periosteal surface but also from the Haversian 
canals. The stages of the bone destruction in the medullary 
part of the bone are shown in figs. 55 and 56. 

The main features of the condition of the bone in advanced 
cases are shown in fig. 57. 

Znamensky remarks that the bone changes are identical with 
those occurring in other diseases, for example, osteomalacia, 
rickets, tabes dorsalis, atrophy of old age, &c. 

Talbot in his excellent work on " Interstitial Gingivitis" gives 
a series of illustrations depicting the microscopical anatomy of 
periodontal disease in dogs. He shows that the earliest mani- 
festation of the disease is in the gingival margin, and that, as 
the disease progresses, both the periodontal membrane and the 
bone become involved. Talbot also gives illustrations of the 
disease in man, and his researches, which confirm the work of 
Znamensky, show that the changes in the bone are of the 
character of a rarefaction or osteoporosis which commences at 
the margin of the tooth sockets. The microscopical investiga- 
tion of the disease thus confirms the conclusions arrived at by 
those who have investigated the macroscopical anatomy of the 
disease in man and other animals. 


The Clinical Appearances of Periodontal Disease. 

The gums normally fit close around the necks of the teeth, 
the spaces between the teeth being filled with tags of gum — 
the interdental papilla, 1 . 

The earliest indication of the disease is a slight congestion of 
the interdental papillae, and even at this early stage the gum 
attachment will be found to be partially destroyed, as may be 
proved by passing a probe into the interproximal space-. 

As the disease progresses the whole of the gingival margins 
become congested and bleed readily; the interdental papillae 
disappear and the normal festooned arrangement of the gum 
around the tooth is lost. An examination of the teeth at this 
stage will usually disclose food and other debris in the approximal 
spaces, while small nodules of calculus are generally present on 
the teeth. Compression of the gums will cause a small quantity 
of discharge to escape at the sides of the teeth. Eventually the 
bone becomes involved in the inflammatory process and is 
gradually destroyed together with the periodontal membrane. 
The gums recede, but the recession does not usually proceed so 
rapidly as the destruction of the alveolar process, and the result 
is that, around the teeth, deep pockets are formed, in which 
pus and other morbid material accumulate and aggravate the 

This stage is characterized by the following condition : The 
mucous membrane appears deeply congested ; the gums are 
swollen at their free margins and bleed readily on the slightest 
touch ; the roots of the teeth are more or less exposed, and 
covered with a layer of hard greenish-brown calculus ; there is 
a foetid discharge and the breath has a repulsive odour due to 
indol-forming organisms. A sickly, sour odour of the breath 


is noticeable when yeasts and bacteria causing carbohydrate 
fermentation are present. The teeth are freely movable and may 
become so loose that they can be removed quite easily. If the 
disease is left untreated the teeth are lost one by one, and 
with the loss of the teeth the inflammatory process completely 

The disease usually progresses with varying rapidity, and 
while the inflammation at one period may be acute with a free 
flow of pus, at a later period its progress may be slow. The 
activity of the disease varies around different teeth ; in some 
cases the greater activity is around the posterior teeth and in 
others around the incisors. 

In some cases the margin of the gum is thickened and in 
a few instances well-marked bosses of bone are present on the 
outer aspect of the alveolar process. To a great extent the 
clinical appearances of the disease vary according to the general 
condition of the patient, the resistance of the tissues, and the 
hygiene of the mouth. 

The disease, especially in advanced cases, is usually associated 
with congestion of the tonsils and the mucous membrane of the 
mouth and pharynx. Superficial glossitis is often present. The 
patient experiences an unpleasant taste in the morning. There 
is frequently recurring haemorrhage from the gums, which is 
swallowed during the day, but occasionally escapes from the 
mouth at night and stains the pillow. The last symptom 
deserves special attention, as there is some clanger that it may 
be mistaken for haemorrhage from the lungs. 

Careful attention to the hygiene of the mouth will not only 
prevent the spread of gingivitis but will also prevent the deposit 
of calculus around the necks of the teeth, as the formation of 
stagnation areas at the gingival margin is favourable to the 
deposit of calculus. 

Mouth-breathers are specially liable to gingivitis, but if the 
tissues react strongly the margin of the alveolar process is 
thickened and the pockets around the teeth as a rule are not 
deep. The type of the organism present naturally influences 
the type of toxins produced in the pockets and so affects the 
rapidity of destruction of the tissues. 



It is not safe to judge the extent of the disease from clinical 
appearances only, and it is necessary to call in the aid of 

Fig. 58. 

Fig. 59. 

skiagraphy in order to ascertain how far hone destruction has 
proceeded. This is illustrated in the following cases. 

The case shown in fig. 58 depicts an early stage of the disease. 


4 1 

Clinically there was no recession of the gums beyond a partial 
disappearance of the interdental papillae between the lower 
incisors. There was a marked marginal gingivitis together with 

Fig. 60. 

Fig. 6i. 

a congestion of the whole of the gums and a free discharge from 
the pockets around the teeth. The arch was well developed and 
there was marked attrition. 



The skiagrams (fig. 59) show that the alveolar process was 
involved and that the destruction of the bone had advanced 
to a considerable extent in the lower incisor region. 

Fig. 62 


Fig. 63. 


The clinical appearances in the case shown in fig. 60 suggest 
a more advanced condition of the disease than in the preceding 
ca>e. The muco-periosteum is more swollen and congested. 


The interdental papillae have disappeared and the gum margin 
on the labial aspects of the teeth just fails to cover the necks ot 
the teeth. The skiagrams (fig. 61) show that the bone destruc- 
tion is much more advanced than the gum recession would 
seem to indicate. 

The case shown in fig. 62 illustrates an advanced condition. 
The skiagrams (fig. 63) show the extensive destruction of the 
tooth sockets. Those marked (a) and (/>) also illustrate a point, 
namely, that the calculus extends only very slightly below the gum 

Fig. 64. 

The case shown in fig. 64 illustrates some features which are 
of interest from the point of view of prognosis. The patient, 
a man, aged 34, was a compositor by trade, and attended the 
out-patient department for dyspepsia. 

Beyond a well-defined marginal gingivitis the gums were 
normal in colour and firm in consistency. The teeth were 
smothered with calculus, the gum margin was above the necks 
of the teeth, and the interdental papilla; had disappeared. 
Examination with a probe showed slight pockets around the 

From the clinical appearance it would be inferred that the 
disease was of slow progression and that there was comparatively 
little bone destruction. 

The skiagrams (fig. 65) show that the bone destruction is 



proceeding with the same rapidity in all parts of the mouth, 
and that the inflammatory process extends only slightly beyond 
the margin of the bone. 

Fig. 65. 




* "'^T^IjJa 


B^^^-^_ } 

Fig. 66. 

In the case shown in fig. 66 the patient was a mouth- 
breather and complained of bleeding from the region of the 
mandibular incisors. The teeth had been regularly cleaned. 
The gums were well up to the level of the necks of the teeth and 
the interdental papillae were not destroyed ; there was no gingi- 



vitis except around the mandibular incisors where pus was 
present. An examination with a probe showed extensive destruc- 

Fig. 67. 

Fig. 68. 

tion of the alveolar process in the region of the mandibular 
incisors,, while in the rest of the mouth the bone was intact. 
The skiagrams shown in figs. 67 and 68 illustrate these points. 

4 6 

The Pathology of Periodontal Disease. 

Considerable light has been thrown on the pathology of 

periodontal disease by studying the disease in animal-. The 
study of a certain disease in the animal kingdom will often assist 
us in arriving at a truer conception of the same disease when 
attacking man. This is certainly true of periodontal disease, and 
it will therefore be an advantage, before discussing the problem 
as affecting man, to pass in review the facts we know regarding 
the pathology of the disease in the lower animals. 

(i) HoKSES. — In the earlier description of the morbid 
anatomy of the disease in the horse the initial lesion was 
shown to be a slight destruction of the interdental papillae 
probably from the injurious character of the food. The injury 
is usually found on the buccal side in the maxilla and on the 
lingual side in the mandible. Food and other matter soon 
accumulate at the injured spot and stagnation areas are formed. 
Organisms already present or freshly introduced into the mouth 
add infection and the toxins produced cause further destruction 
of tissue. The stagnation areas are thus increased, and the tissue 
destruction is accelerated. The infection tends to spread, in the 
maxilla, to the antrum, and, in the mandible, to the body of the 
bone leading in both cases to suppuration. 

In the stagnation areas the teeth become painful to pressure 
and the function of mastication is naturally transferred to other 
areas, with the result that the accumulation of food debris around 
the affected teeth is promoted. 

In the horse the disease is local in origin and is primarily 
due to traumatic injury. Subsequently the lesion spreads partly 



from trauma arising from the tightly wedged accumulation of 
food debris and partly from toxins produced in the stagnant 

(2) Cats and Dogs. — Periodontal disease is exceedingly 
prevalent among domestic cats and dogs. Mr. H. Gray, who 
as a veterinary surgeon has had a wide experience of the 
disease in cats, is of the opinion that the highly bred pet animals 
which are fed on soft food are much more susceptible to attack 

P^ { * *^ 


FlG. 69. — Filis domes/ ica (cat). Appearance of normal gums. 

FlG. "]Q.—Fclis domes/ica (cat). The gums show a marginal gingivitis. 

than the ordinary domestic cat icd on a meat diet, the latter 
being comparatively free from the disease. The explanation is 
that the soft diet clings about the teeth, stagnation areas are 
formed, and a marginal gingivitis is produced. Such a condition 
is well shown in figs. 69 and 70. 

Destruction of the tissues forming the tooth socket follows 
as a direct result of injury from toxins produced in the stagnant 

Among dogs the disease is met with most often in the 
pampered lap dogs and in the short-muzzled breeds of dogs, 


such as the pugs and bull-dogs, and as a rule it is the non- 
functional teeth that are affected, namely, the incisors. In the 
long-muzzled types the disease very commonly starts in the 
region of the second and third maxillary premolars. Generally 
speaking, therefore, the disease commences in dogs in positions 
where soft food is apt to rest, and, as dogs that feed on flesh 
are invariably free from the disease, it is only reasonable to 
inter that in dogs, as in cats, the initial lesion in the gingivae 
is to be attributed to the lodgment of food debris. 

(3) Wild Animals. — Periodontal disease is common in wild 
animals kept in captivity. It is found in rodents, monkeys, 
marsupials, herbivores, and the carnivores. On the other hand, 
the disease is uncommon in animals living in the wild state. 

It will be noticed that in the skulls of captive animals 
aitected by the disease the bone destruction is usually farthesl 
advanced around the areas where the greatest force of mastica- 
tion is exerted and consequently where the soft tissues surround- 
ing the teeth are most liable to injury. The frequency of the 
disease in captive animals and the comparative immunity of 
animals in the wild state, taken in conjunction with the limita- 
tion of the disease to the masticating area, point to the disease 
being closely associated with the character of the food given to 
captive animals. This food is generally of a softer character, 
needing less rending and tearing than the food which the 
animals would obtain in the wild state, consequently the teeth 
are less used and the natural cleansing operations are not per- 
formed. When captive wild animals are given food of a 
character similar to their natural food, as in the case of the 
large carnivores which are fed on a diet of fresh meat, thev 
are almost entirely free from the disease. 

Thus, from a study of the teeth of animals we are led irre- 
sistably to the conclusion that the disease originates locally 
through food lodgment, the tissues being damaged by the fer- 
mentation and putrefaction of the food. This view obtains 
additional support from the condition of the gums and teeth of 
cattle in parts of America where a lesion of the gums frequently 
occurs owing to the penetration of the tissues by the barbed 



crowns of Hordeum jubatum, leading to destruction of the teeth 
sockets and loss of the teeth. 1 

Talbot 2 states that interstitial gingivitis is very common in 
cows fed upon brewers' slop and confined indoors. The slop 
diet accumulates about the teeth and directly injures the gingival 

Fig. 71. 

(4) Man. — If a cover-slip preparation is made from a case 
of periodontal disease a very heterogeneous collection of 
organisms will be found. In fig. yi such a preparation is seen, 
under the dark ground illumination, and Dr. Penfold, who kindly 
examined the slide, states that the following types of organisms 
are present : — 

(1) Treponemata of macrodentium and microdentium varie- 
ties, so-called spirochetes of the mouth. 

1 " Dental Surgery," by Tomes and Novvell, p. 648. 

2 " Interstitial Gingivitis," p. 126. 



(2) Vibrios and spirillary forms. 

(3) Bacilli in great variety. 

(4) Filamentous forms. 

(5) Cocci of various sizes, the grouping of which cannot be 
determined without cultivation methods. 

The large round bodies in the preparation are blood cells. 

The discharge from the same pocket was examined by means 
of transmitted light and revealed the presence of Entamoeba 
buccalis ; a drawing of four stages of one amoeba is reproduced 
in fig. 72. 

Fig. 72. 

The organisms generally present in cultures made from cases 
of marginal gingivitis are staphylococci, streptococci, with at 
times the Micrococcus catarrhalis and the pneumococcus. 

In a series of thirty-three cases recorded by Eyre and Payne 1 
the following organisms were regarded as responsible for 
periodontal disease : — 


Micrococcus staphylococcus pyogenes aureus ... ... ... ... 2 

Micrococcus catarrhalis ... ... ... ... ... ... 9 

Micrococcus catarrhalis and Streptococcus pyogenes long us ... ... n 

Streptococcus pyogenes longus 

Streptococcus lanceolatus pneumonia- (pneumococcus) ... ... 4 

In a more recent communication Dr. L. S. Medalia 8 gives 
the results of his study of 115 cases. He found that the 
organism most frequently met with was the pneumococcus 
{Streptococcus lanceolatus pneumonia), 107 times out of 115. 
The results of his investigation are as follows: — 

1 /'roc. Roy. Soc. Med. (Odont. Sect.), vol. iii, p. 36. 
5 Dental Cosmos, 191 3, p. 24. 



Pneumococcus slrepto-lanceolatus pneumonia ... ... ... 26 

„ and staphylococcus ... ... ... ... ... 67 

,, and streptococcus ... ... ... ... ... 3 

„ staphylococcus and streptococcus ... ... ... 10 

,, and Micrococcus catarrhalis ... ... ... ... 1 

Staphylococcus and Micrococcus caiarrhalis ... ... ... ... 2 

Staphylococcus aureus ... ... ... ... ... ... 2 

Streptococcus and staphylococcus ... ... ... ... ... 1 

Sterile ... ... ... ... ... ... ... ... 3 

From the foregoing it will be noted that the germs found 
in the pus from cases of periodontal disease are the same as 
those responsible for ordinary suppuration in other parts of 
the body. 

Noguchi 1 has shown that in the mouth there are two definite 
varieties of spirochetes, the Spirochcvte microdentium and the 
S. macrodentium, and Drs. J. G. and D. Thomson 2 have shown 
that in severe pyorrhoeas spirochaetes are usually present. 

Recently Barrett and Smith, Bass and Johns, and others have 
called attention to the frequency of the association of amoebae 
with pyorrhoea alveolaris, and it has been claimed that the cause 
of periodontal disease is Endamocba buccal is. In 1849 Gros 
first observed amoebae in the mouth. Sternberg (1862) found 
them in the sordes about teeth. 

The active forms of A. buccalis are from 6 /x to 32 jh in 
diameter; they average about 15 p. They have a distinct ecto- 
plasm, well seen when the organism is in motion ; it is hyaline 
and refractile. The endoplasm is granular and shows many 
food vacuoles, but no contractile vacuole. The nucleus is well 
defined and shows a thick greenish membrane containing a great 
deal of chromatin. A small centriole is situated near the centre 
of the nucleus. The motility is sluggish and the pseudopodia 
are blunt. The cysts of the organism have never been seen in 
the mouth. The above description is accepted by the American 

1 Journ. Exper. Med. 

2 Proc. Roy. Soc. Med., vol. vii, No. 9. Some researches on spirochaetes 
occurring in the alimentary tract of man and some of the lower animals. 


There is, however, little doubt but ihat the amoebae of the 
mouth are of more than one species. The points in favour of 
the amoeba being the cause of the disease are : (i) Its frequent 
association with the disease ; (2) its power to phagocyte red 
cells, a power not possessed to any degree by free-living amoebae ; 
(3) improvement in the local conditions stated to follow the use 
of emetine; (4) the resemblance of the A. buccalis to Entamoeba 
histolytica, the cause of amoebic dysentery. 

The points against A. buccalis being the cause of the disease 
are: (1) The constant association with the disease of other 
organisms, e.g., spirochetes or pneumococci; (2) emetine treat- 
ment removes the amoebae but does not cure the condition ; 
(3) the disease has never been produced by inoculation of a 
suitable animal with a pure culture of the organism. The ques- 
tion is still undecided, but the pyorrhceal pocket may very well 
be simply a favourable environment for the growth of free- 
living amoebae. 

To sum up, investigations into the bacteriology of the disease 
do not afford any evidence of its being due to a specific 

With this brief survey we must leave the bacteriology of 
the disease and consider the condition known as marginal 
gingivitis, an affection which is the forerunner of periodontal 

The removal of all debris is brought about and the gingival 
margins kept in a healthy condition by — 

(1) Efficient mastication of suitable foods. 

(2) Friction of lips and cheeks against the gum margins. 

(3) Movement of the tongue against the teeth. 

(4) Free flow of currents of saliva. 

Abnormal conditions, such as mouth-breathing and function- 
less teeth, lead to the accumulation of food debris, &c, at the 
gingival margin ; the material thus lodged undergoes fermentative 
and putrefactive changes, the soft tissue is injured, and inflam- 
matory reaction follows. In mouth-breathers this process can be 
plainly seen. If the mouth of a child suffering from nasal 
obstruction be examined, a marginal gingivitis will be found 


around the anterior maxillary and mandibular teeth, while the 
gingival margin at the posterior part of the mouth will be found 
quite healthy, provided, of course, that the function of mastication 
is properly performed. With mouth-breathing the natural 
friction of the lips against the gums is, to a great extent, in 
abeyance, and the result is that the debris around the teeth is not 
removed and the gingival margin is injured. The gingivitis so 
often associated with many fevers arises, partly at least, from 
a similar cause. The fevers frequently give rise to a condition 
which induces mouth-breathing, and, a " slop " diet being 
necessary, the ordinary functions of the mouth are not performed 
and food naturally collects at the gingival margins. If the 
marginal gingivitis persist, the periodontal membrane becomes 
involved and the condition known as periodontal disease 

In non-mouth-breathers the disease commences in the molar 
region and gradually spreads to the anterior teeth, while in 
mouth-breathers the disease commences earlier in life and is not 
infrequently confined for some time to the anterior teeth. Thus 
in the non-mouth-breathers the disease commences in the region 
where lodgment of food is liable to occur and the initial lesion is 
probably an injury to the gingiva? from food debris. In other 
words, the disease commences precisely in those positions where 
stagnation areas are most likely to form ; a marginal gingivitis is 
started and in time the periodontal membrane becomes involved, 
the tissue destruction following exactly the same course as in the 
lower animals. 

The initial lesion in man is injury to the gingival margin 
leading to the formation of a stagnation area. From the material 
which collects in this area toxins are formed and the tissue 
changes which follow are identical with those seen in the lower 
animals. In the area immediately beyond the ulcerating surface 
— for as such it must be regarded — the tissues react and form 
a protecting barrier, and the progress of the disease depends 
on the efficiency of this barrier. The reaction of the tissues 
depends upon — 

(1) Their inherent vitality. 



(2) The degree of functional activity — the greater the flow 
of lymph through the area the greater will be the accumulation 
of antibodies. 

(3) The severity of the infection. 

In many cases of periodontal disease, more especially in 
young adults, the natural defence of the tissues suffices to prevent 
the undue absorption via the bone of toxins or organisms. The 
discharge from the mouth, however, is swallowed with the saliva 
and consequently the gastric mucous membrane is continually 
being damaged. Sooner or later the defence of the tissues at this 

Fig. 73. 

part breaks down and eventually the whole intestinal tract becomes 

The tissues of many patients seem to be incapable of raising 
a sufficiently effective barrier even in mild cases. From the 
pockets around the teeth a direct absorption takes place through 
the periodontal membrane and pathological changes commence 
in the tissues around the apices of the teeth. From these areas 
the toxins pass into the general circulation. 

The view here expressed is well illustrated by the two 
following cases : — 


M. P., single, aged 30. This patient came under observation 
in January, 19 10. The condition of the gums is shown in fig. 73. 
A general gingivitis was present, but the recession of the gum 
margins was slight. 

The pockets around the teeth were moderately deep, the gums 
bleeding readily on the slightest touch. The skiagrams (fig. 74) 
show the condition of the alveolar process in the incisor vegion. 
The patient was a pronounced mouth-breather and occasionally 
suffered from indigestion, but she stated that she generally felt 

Fig. 74. 

well. In 1904 she was assured for ^"100. Scaling and local 
remedies, combined with Bier's treatment, were tried. In July, 
1910, the appearance of the gums had improved, although a good 
deal of gingivitis was still present. Skiagrams taken did not 
show any extension of bone destruction. 

In October, 19 10, the patient developed lung trouble, and 
was treated in a home, and at Easter, 191 1, she had an attack 
of diphtheria. In June the mouth condition w ? as worse, and 
the following teeth were removed : — 

87 5 1 8 

87 I 4 5 7 8 



From the apex of 5j the Micrococcus fetragenus was obtained. 
The removal of the upper and lower incisors was carried out 
early in September. On October 9 the patient stated that there 

Fig. 75. 

Fig. 76. 

had been distinct improvement in her health since the last 
extractions, and she had gained 8 lb. in weight. Skiagrams 


of the alveolar process taken immediately before the extraction 
of the premolars and molars are shown in fig. 75 and of the 
incisors in fig. 76. 

During the treatment skiagrams were taken at frequent 
intervals, and showed very slight increase in the amount of bone 
destruction during the eighteen months of local treatment. The 
teeth removed from this patient showed definite signs of trouble 
round the apices, indicating the presence of a rarefying osteitis 
(see fig. 77). 

In this case there are several points of interest. The 
gingivitis persisted, notwithstanding that the patient paid the 
most scrupulous attention to the cleanliness of her mouth, and 

Fig. 77. 

the lesson to be learnt from this is that no care and cleanliness 
on the part of the patient who is a mouth-breather will remove 
the gingivitis, and therefore the dental sepsis, when once it is 
established. The alveolar process had been only very slightly 
destroyed and this would seem to indicate that the Bier's treat- 
ment had proved of some value, but too much importance must 
not be laid on this point. Another question that presents itself 
is this : If the teeth had been removed early in the previous 
year, would the avoidance of six months of dental sepsis have 
prevented the development of lung trouble ? Lastly, the 
acceptance of this patient as a first-class life raises a point of 
considerable interest in social and commercial circles. The 



patient is suffering from an incurable condition of marked oral 
sepsis which is admittedly one of the most important etiological 
factors in the whole realm of pathology, and the question very 

Pig. 78. 

Fig. 79. 

naturally arises whether she could properly be regarded as a 
first-class life with such a potential cause of disease present. 
The second case is that of a female, aged 25. She had 


marked general gingivitis and was a mouth-breather. Local 
treatment had been carried on since the previous October. The 
patient complained that she was never without headaches and 
that she felt " terribly shaky down to the bottom of her 
stomach." The slightest exertion made her feel sick. Her 
tongue was coated. Her blood-pressure was 141. Skiagrams 
of this patient are shown in figs. 78 and 79. 

In a few places there were signs of rarefying osteitis. With 
experience of previous cases, and taking into consideration the 
general condition of the mouth and the health of the patient, 
the removal of all the teeth present was advised, namely — 

76 321I1234 78 
654321 j 1234567 

By June 7 the teeth had been extracted and, without exception, 
showed pathological changes at the apex. Towards the end of 
julv the blood-pressure had fallen to 124, the sickness had 
gone, the skin was clearer, and the patient admitted that she was 
feeling much better. By the end of October she had increased 
6 lb. in weight, was feeling very much better, and eventually 
made a complete recovery. The above cases are merely given 
as typical examples of many others. 

Teeth removed from cases of periodontal disease usually 
show a deposit of calculus ; in some cases the deposit occurs as 
a rim of hard calculus just below the neck of the tooth, while 
in others the calculus is freely dispersed over the surface of the 

Many observers attach considerable importance to the 
calculus around the necks of the teeth and regard this as the 
cause of periodontal disease. Dr. Black regards the gingival 
organ as a glandular structure and considers that it possesses the 
function of selecting and eliminating from the blood certain 
poisons, as evinced in mercurial gingivitis. The elimination of 
these poisons leads to inflammatory reaction in the gingival 
tissues, and, partly from the abnormal secretion and partly from 
the inflammatory exudates, the calculus is formed. 

The presence of a stagnation area is, in my opinion, quite 
sufficient to account for the deposit of calculus, and I am 


inclined to regard the deposit as the product of the material 
stagnating in the pockets. When calculus has been deposited, 
drainage of the pockets around the teeth is hindered and the 
calculus consequently increases through stagnation, and the 
progress of the disease is assisted. Clinical evidence supports 
the view that the deposit of calculus is the result and not the 
cause of the gingivitis. 

The view that the disease is intimately associated with the 
deposit of urates in the periodontal membrane does not seem 
to be tenable in the light of facts obtained by recent observers. 
Dr. Pierce, who is the main advocate of this view, states that the 
salts are most frequently deposited near the region of the apex 
in the form of calcium and sodium urates with traces of uric 
acid and calcium phosphates. The deposit causes irritation, the 
tissues break down, an exit is formed for the pus around the 
neck of the tooth, and infection of the mouth ensues. 

In connection with this contention it must be remembered 
that gout is essentially a non-suppurative disease and gouty 
deposits in the hands, ears, &c, do not promote suppuration. 
It is extremely doubtful whether the so-called gouty peri- 
odontitis can be regarded as a clinical entity. It is probable that 
the appearances seen in patients of a gouty diathesis are due to 
a chronic injury of the periodontal membrane of low intensity 
and that the adjacent tissues react and give rise to the clinical 
appearances classed as gouty periodontitis. 

In considering the pathology of periodontal disease, careful 
attention must be given to the degree of resistance of the osseous 
tissues, which has probably a very important bearing on the rate 
of progress of the disease. From an examination of dried 
specimens it would certainly appear that the more compact the 
osseous tissue the greater the barrier to the spread of the disease. 
The question arises whether the tissues of the tooth socket are 
as resistant to disease as might naturally be expected. We are 
without any trustworthy data bearing on this point, but there 
are certain phenomena which tend to show that in many people 
the tissues lack normal resistance. It is a well-established 
principle that no part of a living creature can be maintained 


in a healthy condition when it ceases to perform its appointed 
functions, and, beyond doubt, under modern conditions the 
normal functions of the teeth and surrounding tissues are not 
performed. The consequence is that the tissues are deprived 
of a normal blood supply and their vitality is diminished. As 
the bone surrounding the teeth is a tissue of transient structure, 
depending for its very existence on the teeth themselves, it is 
only reasonable to assume that the growth of the bone tissues 
is very largely dependent on the functional activity of the teeth. 
Modern diet is such that the full functional activity of the teeth 
is seldom brought into play, much of the food requiring very 
little mastication, and this loss of the function of the teeth must 
seriously affect the structure of the bone forming the alveolar 
process and render it less resistant to attack. Clinical observation 
supports this view. In mouths which show that the function of 
mastication is duly performed the alveolar process is well deve- 
loped, and if periodontal disease attacks such mouths its progress 
is not rapid. On the other hand, if mastication has been imper- 
fectly performed, the bony coverings of the teeth are thin and 
sparse, and the disease, when once 'Started, progresses rapidly. 

There is another point to he considered in conneetiamwith 
the resistance of the tissues of the bene; viz., that any inimical 
condition affecting the osseous system fe like' show .itself in 
the alveolar process at an early age, the reason being that, as 
already explained, the alveolar process is a transient structure. 


The Etiology of Periodontal Disease. 

Considerable diversity of opinion exists as to the cause 
of chronic general periodontitis. 

In reviewing the pathology of the disease in animals it has 
been shown that the lesion was caused by injury from the food. 
When cats and dogs are fed on a diet of fresh flesh thev are 
invariably free from the disease, but as soon as soft pap food is 
substituted the animals become a prey to the disease. 

In the horse the disease can clearly be traced to injury from 
the food, the particular form in which the food is given being 
responsible for the injury. Under natural conditions horses 
feed upon grass which, being torn up in long strands and in 
a pliable state,- can be nrasticate'd U-id disposed of without injury 
tor the soft tissues. '^'Lfnder "civilized" conditions horses fre- 
quentlycannot- be put' out' to grass and the food is often given 
in the form -of hay and straw (chaff) cut up into short lengths. 
Chaff in short' 'stiff 'lengths is very likely to cause injury to the 
muco-periosteum 'through being pressed into spaces between the 
teeth. This view of the causation of the disease in horses is 
supported by the fact that the disease is prevalent wherever the 
conditions are such that fragments of thorn become mixed with 
the food. Similarly, as previously mentioned, cattle in parts of 
America are subject to the disease owing to the penetration of 
the tissues by the barbed crowns of Hortleiun jubatum. 

In the horse the disease is clearly to be attributed in a very 
large measure to alteration in the physical character of the food. 

In man, too, the evidence points to the disease being started 
by injury of the gingival margin from food debris, or the local 
action of toxins as seen in the marginal gingivitis of mouth- 


The prevalence of the disease is probably due to the character 
of the diet of the present day. Much of our food is now prepared 
in such a manner that it readily accumulates around the teeth 
and is of a character which easily undergoes fermentation. The 
food thus prepared requires but little mastication, with the result 
that the tissues in and around the teeth are deprived of an 
adequate blood supply and are thus rendered less resistant to 
attack. Evidence in favour of this is shown in a series of skulls 
of Londoners of the sixteenth and seventeenth centuries. Peri- 
odontal disease in the region of the molars is extremely common 
in the skulls, but the disease is chronic in character and the 
bone shows distinct reaction to injury. In the majority of these 
skulls the function of mastication was efficiently carried out as is 
shown by the attrition of the teeth. As soon as the disease has 
started, the formation of abnormal pockets favours the accumula- 
tion of debris, and so the action of the toxins is accelerated. 

It is necessary here to consider wherein lies the difference 
between caries and periodontal disease, seeing that both are 
traceable to the lodgment of food. It is probable that the 
deciding factor is the predominance of particular foodstuffs. 
On carbohydrates enzyme action results in the production 
mainly of lactic acid, while on proteins enzyme action results in 
the formation of ptomaines which are alkaline in reaction. 

If we turn to the food of modern times we notice a very 
distinct increase in the number of made-up dishes with a corre- 
sponding decrease of plain fresh-cooked food. A large proportion 
of the animal food is imported and has been kept in an ice- 
bound condition. Such food undergoes putrefactive changes 
more quickly than fresh animal food. 

Attention has been drawn to the intimate relationship between 
periodontal disease and mouth-breathing, and the increase in the 
number of individuals who are'mouth-breathers has, undoubtedly, 
added to the increase of the disease. 

6 4 


Periodontal Disease as the Active Agent in the Production 
of Pathological Lesions. 

It is now generally admitted that periodontal disease may 
be the starting point of various other pathological lesions, and 
it is proposed, therefore, to review this subject broadly, and to 
make special reference to certain diseases which seem to be 
frequently traceable to mouth infection. A full and detailed 
discussion of this question would be beyond the scope of the 
present work and would necessitate too deep an incursion into 
the realm of general pathology. 

(A) The Normal Condition of the Alimentary Canal. 

In the normal mouth the teeth are arranged in a regular 
arch ; the gums are firm and of a light pink colour, and are 
attached to the teeth at their necks. In the process of mastication 
food tends to cling about the teeth, especially around the necks 
of the teeth where the gingival margin is attached in such a way 
as to leave a slight trough, but when normal conditions prevail 
the mouth is quickly freed of food debris by the combined action 
of the cheeks, tongue and saliva. 

In the healthy mouth certain organisms are always present. 
The majority of these organisms cannot be grown in ordinary 
culture media, and, of those which can be grown, the strepto- 
cocci are in " overwhelming preponderance." When food is 
being taken, and probably at other times, adventitious organisms 
are introduced into the oral cavity. 

Various factors contribute towards the maintenance of the 
"bacteriological balance" in the mouth, e.g. (i) the mouth 


is constantly flushed with saliva which carries the organisms to 
the stomach. (2) Phagocytes are incessantly passing up between 
the epithelial cells, and either take up the organisms or discharge 
their bactericidal content ; some, " having performed their func- 
tions, undergo dissolution or are swept away by the currents 
of saliva," while others find their way back into the subjacent 
tissues and are rapidly destroyed. (3) The bacterial struggle 
for existence is probably a contributory factor as suggested by 
the results of Miller's experiments. In one experiment he 
thoroughly rinsed his mouth with a bouillon culture of Bacillus 
prodigiosus containing over 2,000,000,000 bacilli, and found 
that at the end of three hours his mouth was practically free 
of that organism. 

The organisms reaching the stomach from the mouth are to 
a great extent killed or inhibited by the action of the gastric 
juice, and a few hours after meals the duodenum may be found 
quite sterile. In the small intestine bacterial growth starts 
afresh, the rate of growth increasing as the colon is approached; 
at the colon bacterial multiplication reaches its maximum. The 
bile exercises a selective action on the organisms, and, while 
checking the growth of certain organisms such as the delicate 
streptococci, the pneumococci and the Bacillus proteus, has no 
effect on the typical intestinal bacteria such as the B. coli group 
and the hardier streptococci. The bacteria in the intestines are 
disposed of in two ways. Some are expelled with the faeces, 
and these are probably the majority, while others find a passage 
through the intestinal wall. The latter are arrested either in the 
subcutaneous lymph nodules, or, evading these, are either 
trapped in the mesenteric and retroperitoneal lymph glands, 
or reach the venous radicles of the portal vein where the 
endothelial cells arrest the leucocytes with the contained bacteria. 

With regard to the toxic products of the bacteria, it is, says 
Andrewes, 1 " conjectured that such injurious substances absorbed 
from the alimentary canal as may escape the alchemy of the 

1 Discussion on Alimentary Toxaemia, Proc. Roy. Soc. Med., vol. vi, No. 5 



liver are neutralized by the secretion of certain of the ductless 
glands — for example, the thyroid." 

Briefly, it may be said that under normal conditions the 
organisms in the alimentary canal are efficiently dealt with by 
the body defences and their presence causes no ill-effects. 

(B) Abnormal Conditions of the Alimentary Canal. 

Any septic condition of the mouth adds fresh organisms, 
the normal flora being increased and new varieties appearing. 
"The abnormal products of tissue reaction to injury are present, 
that is, inflammatory exudation which is rich in proteid, and 
an enormous increase of dead cells, epithelial and otherwise." 
The abnormal flora in conjunction with abnormal environment 
modify the virulence of the organisms in the direction either of 
attenuation or of exaltation. 

The local effect of this increase of organisms is to undermine 
and weaken the epithelial covering, which then affords a passage 
for the organisms into the deeper tissues, and, in periodontal 
disease, where the organisms and their product are stagnant in 
the " pockets," the organisms constantly pass into the medulla 
of the bone and are absorbed into the general circulation. This 
latter condition is manifestly present where there is marked 
rarefying osteitis, and is probably also present in many cases 
where there is but little bone destruction. This question was 
referred to on p. 54. 

The presence of an increased number of organisms and their 
toxins in the stomach generally results in a gastritis, which in its 
turn lessens the efficiency of the gastric defence, and an over- 
whelming number of organisms pass into the small intestines. 
Under these conditions the defences of the intestines are taxed 
to their uttermost, and a greater number of organisms pass 
from the intestinal surface into the system. In the opinion of 
Adami this condition often leads to a sub-infection rather than 
an active infection. " The bacteria carried in do not multiply 
and set up foci of suppuration ; they are destroyed, but with 
their destruction the liberation of their toxins causes a poisoning 


of the cells immediately around them, and the accumulative 
action of these toxins, whether locally or at a distance, upon the 
liver cells, for example, brings about the death of certain cells 
and replacement by fibrous tissue." 

The toxic products of the bacteria are also increased, and, as 
the normal defences are unable to neutralize them, they pass 
these defences and are distributed to the tissues, attacking those 
cells for which they have the requisite chemical affinity. In this 
manner the organisms or their toxins are absorbed into the blood- 
stream either directly via the bone or indirectly via the intestinal 
canal, and the pernicious influence of periodontal disease thus 
passes deep into the system and starts other diseases. 

The disease which results from the infection of the blood- 
stream varies in different individuals. The reason that the 
resulting disease takes different forms in different individuals 
is not far to seek and has been well explained by Dr. Stanley 
Colyer as follows : "In all diseases there are always two factors 
at least, the seed and the soil, without which disease cannot exist. 
The seed varies, the soil varies ; never are the two the same ; 
never is the relation repeated. This is why variation in disease 
occurs, and in no two persons does it run a precisely similar 
course. Oral sepsis is but a comprehensive term to include 
various forms of septic conditions of the mouth, it is not 
a disease. The germs causing the sepsis vary, and so the germs 
passing into the body and the toxins absorbed produce different 
results in different people. It cannot be said precisely why 
germs of a particular kind entering one body produce a septic^ 
aemia, and in another an infective endocarditis ; or why a toxin 
in one will produce anaemia, and in another a neuritis ; that 
such is the case, however, seems comparatively certain, and one 
must rest content for the moment with the fact." 

Caution is necessary in assuming that periodontal disease 
is the cause of some other disease with which it is associated 
until all other possible sources of infection have been eliminated, 
But even where sepsis in the mouth is not the primary cause, 
it must not be neglected ; otherwise, by lowering resistance, 
it will assist the pathological process. 


(C) Diseases associated with Periodontal Disease. 

Certain conditions seem to be closely connected with peri- 
odontal disease. Chronic inflammatory changes in the oro- 
pharynx, if not directly due to the persistent infection from the 
tooth sockets, are undoubtedly markedly affected by it. Amongst 
those conditions chronic glossitis is of special interest because of 
the marked tendency for this condition to pass into carcinoma. 

Syphilis is usually regarded as the principal cause of chronic 
glossitis, but, where there is no dental sepsis, there does not 
appear to be any special tendency for syphilitica to develop 
chronic glossitis, whereas when dental sepsis is added chronic 
glossitis usually develops. 

For years past it has been recognized in surgical practice 
that there is a very great tendency for carcinoma of the tongue 
to develop in patients with chronic glossitis and a history 
of syphilis. During the last three years cases in which the 
tongue began to show suspicious appearances and in which 
all sources of dental sepsis were then removed by extraction 
of the teeth have been watched, and in every instance the 
removal of the sepsis was followed by marked improvement. 
These facts certainly point to an intimate connection between 
dental sepsis and carcinoma of the tongue. 

There is ample evidence to show that oral sepsis and 
gastric affections are closely connected. In many instances 
the gastric condition is the direct result of the constant pre- 
sence of septic saliva, and cases are constantly occurring in 
practice in which, with the removal of the oral sepsis, the gastric 
condition completely clears up. In such cases the chain of 
events is probably as follows : The food, imperfectly masti- 
cated and incorporated with septic saliva, undergoes excessive 
fermentation, with the result that, sooner or later, a catarrhal 
inflammation of the gastric mucosa is started. The chronic 
gastritis is probably of the mucous variety in which the acidity 
is always slight, a point of considerable importance as far as the 
inhibition of the microbes is concerned. The catarrhal inflam- 
mation is kept alive by the constant presence of the septic 
matter, and may become infective in character. There is reason 


to believe that sepsis from the mouth is the cause of ulcer of the 
stomach found in old people ; but the gastric ulcer seen in young 
girls no doubt arises from some other cause, as, in a large 
proportion of the latter cases, the mouths are clean. But in all 
cases of gastric ulcer, whatever the cause, it is probable that 
healing would be retarded or prevented while oral sepsis is 

As pointed out above, the gastric juice under normal condi- 
tions inhibits or destroys the majority of organisms entering 
the stomach, and consequently the number passing into the 
duodenum is relatively small. But the bactericidal power of the 
gastric juice is diminished in cases of gastritis and there is then 
an increase in the number of organisms passing through the 
pyloric opening, and a greater risk of infection in the small 

The gastritis may be of an infective character, and a case 
of this kind is quoted by Dr. Hunter 1 who considered that the 
gastritis was distinctly traceable to the mouth condition. The 
history of the case was as follows : — 

"This was a case of subacute gastritis in a woman, aged 62. 
The patient suffered from severe intermittent sickness and gastric 
pain, necessitating the use of morphia, lasting eight months, with 
loss of weight and increasing weakness. Cancer was suspected, 
but on examination no sign of malignant disease was visible 
in the stomach, the abdomen, the rectum, or the uterus. 
Constant complaint was made of a bitter taste in the mouth, 
nausea, and loathing and distaste for food. The vomit in this 
case was loaded with streptococci, staphylococci, and a few 
bacilli. The only teeth present were three roots, around which 
there was a free discharge of pus. With the removal of these 
teeth the gastric condition rapidly improved." In this case it 
would seem that the mouth condition was responsible for 
the infection of the gastric mucosa which, owing to persistent 
damage, had been deprived of its natural powers of resistance 
and so rendered susceptible to attack. 

1 Lancet, January 27, 1900. 


There is every reason to believe that a duodenitis may result 
from the increased number of organisms passing through the 
pylorus, and that the infection may spread along the common 
bile-duct and cvstic duct to the gall-bladder. In this manner 
a chronic cystitis may be started, a condition which, pathologists 
maintain, is necessary for the formation of gall-stones. It seems 
probable that infection may spread along the pancreatic duct 
and give rise to a pancreatitis which will cause pressure on the 
common duct and thus lead to jaundice. This view is supported 
by the fact that, in many cases of jaundice, Cammidge's pancreatic 
reaction may be obtained. The passage of the toxic products 
from the stomach, in addition to starting a duodenitis, may lead 
to an enteritis and possibly colitis. P. Daniel : maintains that, 
in cases of oral sepsis, the lower part of the ileum is always in an 
infected state. 

When a general gastro-enteritis has been established, toxic 
matter will be produced in abundance, which, on being absorbed, 
will initiate various general lesions. 

To sum up briefly, it would seem that oral sepsis leads to 
gastritis, and that gastritis leads directly or indirectly to a general 
inflammation and infection of the intestinal canal. It is in the 
intestine that the toxins are produced in greater quantity, and it 
is from this area that they are mainly absorbed. 

It is quite true that many patients under 40 years of age, who 
have suffered from periodontal disease for several years, may 
show no signs of gastro-intestinal disease ; but, after that age, 
periodontal disease undoubtedly gives rise to gastro-intestinal 
trouble in a very large number of cases. The explanation is that 
up to the age of 40 the body resistance successfully combats the 
abnormal gastric condition, but after that age the body resistance 
gradually diminishes and infection results. 

As the abnormal conditions started in the oro-gastro-intes- 
tinal canal by periodontal disease may be regarded as the result 
of direct infection, we will next consider some of the patho- 
logical conditions created by the continuous passage of the 

1 Lancet, January 15, 1910. 


bacteria into the tissues, or the absorption of toxins from the 
diseased oro-gastro-intestinal canal. One of the commonest of 
these conditions is that of " chronic ill-health." There is a lack 
of energy, a general condition of malnutrition ; a sallow, un- 
healthy appearance in young people, acne pustulosa, and in 
elderly people acne rosacea and eczema, and, invariably, a 
history of gastro-intestinal disturbance. This condition should 
be regarded as the result of the continued absorption of 
small doses of toxins and should be classed as a chronic 
toxaemia. This toxaemia is probably due to : (1) Absorption 
of toxic products of organisms ; (2) absorption of toxins pro- 
duced from abnormal digestive processes. When the source 
of the oral sepsis has been removed there is a rapid improve- 
ment in the gastric condition and the general health ; the 
improvement, be it noted, commencing before the insertion of 

In these cases the extraction of the teeth not only eradicates 
the main source of toxins from the mouth, but also, by removing 
the cause of the gastro-intestinal condition, stops the formation 
and absorption of toxins from that area. 

In practice there is a type of case met with in young adults 
in which there is a loss of weight, accompanied by a constant 
rise of temperature towards the end of the day, and the develop- 
ment of physical signs suggesting tubercle. An examination of 
the sputum fails to demonstrate the tubercle bacillus. I have 
seen several cases in which the symptoms have cleared up 
completely on the removal of the dental sepsis. The following 
is a typical case : A young man, aged 34, developed in October, 
1913, an irido-cylitis, which was diagnosed as tuberculous. For 
some time previous to this he had been generally run-down, and, 
shortly after the eye lesion appeared he showed definite physical 
signs of early tubercle of the lung, with a rise of temperature 
every evening. Examination of the sputum failed to demonstrate 
the presence of the tubercle bacillus. He was sent away as a 
suspicious case for a prolonged rest by the sea. The medical 
man under whose care he was placed suspected that the eye 
lesion was septic, and he was referred to me to report on the 


condition of the teeth. There was a fair degree of periodontal 
disease with marked gingivitis. The patient was a mouth- 
breather. Removal of the teeth was advised. With the extrac- 
tion of the first batch, four in number, the lung symptoms, 
which had become quiescent, returned together with the evening 
rise of temperature and physical signs in the chest. When these 
had again subsided the teeth were gradually removed, and he 
made a rapid and complete recovery. The eye condition cleared 
up, and the general health showed marked improvement. In 
the following July he was said to be in better health than he 
had been for years, and the improvement was remarked on by his 

This case is of interest from the following points : — 
(i) There was a marked family history of tubercle. 

(2) The lung symptoms were extremely suspicious, and even 
if there was no active tubercle the presence of the oral sepsis 
rendered the patient much more liable to direct tuberculous 
infection. The necessity for a clean mouth was clearly indicated. 

(3) The return of the lung symptoms after the removal of the 
teeth indicated a causal relationship. 

This case, viewed by the experience of others I have seen, 
suggests that in individuals predisposed to tubercle the oral sepsis 
may act by lowering the general vitality, and so increasing the 
liability to tuberculous infection. 

Those ill-defined conditions embraced by the terms " chronic 
rheumatism " and " muscular rheumatism " owe their origin to 
sepsis, and the focus of infection is frequently the mouth. The 
rapidity with which these conditions, often of long standing, 
will entirely clear up with the removal of the periodontal disease 
is truly remarkable. 

The form of arthritis usually classified as rheumatoid arthritis 
is now generally accepted as having an infective origin. In this 
type of arthritis the larger and sometimes the smaller joints of 
the hand and foot are affected, the morbid process having its 
origin in the peri-articular tissues. It is usually met with in 
patients under 40 years of age, and is more common in women 
than in men, but it is seen about equally in boys and girls. 


There is abundant clinical evidence to show that the focus of 
infection is frequently traceable to the mouth, and the rapid and 
permanent recovery which often follows the removal of the 
periodontal disease in these cases clearly shows the intimate 
connection between the two conditions. A word of warning, 
however, must be uttered against prematurely assuming that 
where periodontal disease and rheumatoid arthritis are associated 
they necessarily stand in the relation of cause and effect, as other 
active foci of infection may be present ; for example, the vagina, 
urinary system, &c, which may be the main source of infection. 

The Hunterian lecturer for 1899, Sir Douglas Powell, 
recorded a case of cardiac irregularity which was only slightly 
relieved by a course of Nauheim baths and resistance exercises, 
but which entirely ceased when the teeth had been treated. 
Cases of this character are by no means uncommon, the relief 
to the heart symptoms almost immediately following the removal 
of the septic foci in the mouth. The irregularity of the heart 
may be explained on the assumption of a toxin from the mouth, 
or gastro-intestinal tract, having a specific affinity for certain of 
the cardiac nerves. 

Lastly, mention must be made of the importance of periodont- 
itis as a cause of disease in the eye. This has been fully appre- 
ciated since it was recognized that a focus of chronic sepsis, 
situated in any part of the body, could give rise to an acute or 
chronic inflammation in any of the tissues of the eye, with the 
possible exception of the lens, which may suffer, however, in a 
secondary manner. 

Amongst 215 cases of inflammation of the eye, which Mr. W. 
Lang 1 attributed to sepsis, 129 were caused by periodontitis. 
He found also that the more vascular parts, the iris, the ciliary 
body and the choroid, were affected seven times more frequently 
than the less vascular sclerotic, retina and optic nerve, and only 
in one instance was the cornea primarily attacked. It is probable, 
therefore, that the poison is carried in the blood-stream. 

I am indebted to Mr. Lang for the following account of the 
relations of dental sepsis to eye lesions. 

1 Supplement to Proc. Roy. Soc. Med., May, 19 13. 


As the pathology of these eye affections is still obscure it is 
only possible to prove that these diseases of the teeth and of the 
•eye bear the relationship of cause and effect by selecting cases 
where only one source of sepsis appears to be present, removing 
it and watching the result. In this way and without any other 
treatment recently lost sight has been rapidly regained, and acute 
attacks of inflammation have been cut short and have not 
recurred, whereas in former times, when the source of sepsis was 
not removed, the sight in similar cases was not restored in spite 
of every known treatment and the attacks of inflammation 
recurred until the eye was lost. 

The following is a list of affections which periodontitis 
may cause : — 

Interstitial keratitis. 

Scleratitis and episcleritis. 

Iritis and irido-cyclitis with exudation into the vitreous 
followed by secondary cataract and secondary glaucoma. 

Central choroiditis, which was formerly described as senile 
central choroiditis and was attributed to senility when the patient 
was elderly, though similar disease occurs in young people, but 
not so frequently. 

Disseminated choroiditis, confluent and discrete, which may 
be followed by detachment of the retina. 


Optic neuritis. Progressive myopia and asthenopia. 

Until quite recently these diseases were attributed either to 
gout or to rheumatism, whenever tubercle, syphilis, gonorrhoea, 
diabetes, albuminuria and fevers could be excluded. It is now 
known that they are more frequently due to some septic infection 
in the proportion of thirteen of septic to ten of all other kinds. 
The following instances illustrate this view : — 

Episcleritis. — A patient with this condition which had been 
present for five months recovered after treating the periodontitis. 
It recurred again and after lasting a year all the teeth were 
removed. The next clay the eye was whiter. The general health 
improved and she said " life was worth living," and the eye 
recovered rapidly. Two years later she had appendicitis and the 


episcleritis returned ; both diseases quieted down together and six 
years later neither had relapsed. 

Kcrato-iritis uiih Vitreous Opacities and Secondary Glau- 
coma. — A man, aged 37, with normal vision § in each eye, had 
mutton-fat keratitis punctata and periodontitis, for which he was 
treated. A year later, when he was seen by another surgeon, he 
could only count fingers at two feet with the right and at one 
foot with the left eye. The vitreous was too hazy for the fundus 
to be seen, the tension was raised and the field of vision con- 
tracted in the right eye. Another dentist condemned all the 
teeth and when they had been removed the vision began to 
improve. Three years later the vision in each eye was § and 
SN 0-25'. 

Central Choroiditis. — An officer of the Yeomanry, who 
thought himself to be in good health, noticed two days before 
coming under observation a brown stain on the newspaper. 
On covering one eye he observed a blur which involved the 
fixation point ; this was found to be clue to a small patch 
of central choroiditis which had reduced the vision to | slowly. 
Five days later the brown mist had gone and the vision was f . 
In the interval three septic roots had been removed and his 
periodontitis treated. 

Kerato-iritis, Secondary Cataract and Secondary Glaucoma. — 
A lady, who had suffered from recurring attacks of inflam- 
mation in both eyes for fifteen years, during which one eye had 
been excised and a secondary cataract removed from the other, 
came under observation for attacks of glaucoma, which obscured 
the sight every morning, but cleared again at night, when she 
saw very well. In this state of obscuration which reduced the 
sight to the counting of fingers at a distance of three feet, all 
her septic teeth were removed under a general anaesthetic. On 
regaining consciousness the vision was clear. A year later it was 
reported to be normal and never to have been again obscured. 

Disseminated Choroiditis. — In this patient disseminated 
choroiditis in one eye had reduced the vision in six months 
to a°o. She had all her teeth removed for periodontitis. In 
two days the vision was f ; three weeks later it had gone 


back to 2 S ¥ ; a root which had been overlooked was removed 
the same day and within a few days the vision returned to f. 

Operation for Senile Cataract. — A lady with a septic mouth, 
which she refused to have treated before an operation for 
senile cataract, submitted to having all her teeth removed, 
when an iritis began to cause pain four days after the cataract 
had been extracted. The same day the pain in the head 
and eyes was less, and the inflammation ceased to increase ; 
two days later the gums, which could not be cleaned up before 
the teeth were removed, were foul, and the eye was worse. In 
a few days the gums were clean and at the same time the eye 
improved and recovered very quickly and was well within three 
weeks. In similar cases where the source of sepsis is not 
removed the eye would remain inflamed for many weeks. 

It is not intended that the foregoing should be regarded as 
dealing exhaustively with the special conditions which are trace- 
able to periodontal disease. Medical literature of recent years 
contains numerous references to other conditions having a 
similiar source. But sufficient has been said to demonstrate that 
sepsis around the teeth is a potent source of general infection, 
and that wherever a disease has a septic origin dental sepsis may 
be the cause, or at any rate a contributing cause. It is a little 
difficult to understand why medical men should so often place 
the utmost importance on a small area of sepsis in other parts of 
the body and refuse to recognize the serious source of sepsis so 
often present in the mouth. 


The Treatment of Periodontal Disease. 

In the chapter on the morbid anatomy and pathology of 
the disease, it was pointed out that the formation around the 
teeth of " pockets," which inevitably become stagnation areas, is 
the outstanding feature of the disease. Until these " pockets " 
or stagnation areas have been eradicated, it does not seem 
reasonable to claim that a cure has been effected, and as it 
is almost impracticable to eradicate them actual cures of 
periodontal disease are rare, though well-directed treatment 
may keep the disease in check. Reference has also been 
made to the important role which mouth-breathing plays in 
the promotion of the disease. It has also been shown that 
the progress and severity of the disease is greatly influenced by 
the degree of resistance offered by the tissues. 

Treatment, therefore, should be directed towards promoting 
efficient drainage, raising the resistance of the tissue and ensuring 
proper nasal breathing. 

With regard to the breathing, I am firmly convinced that in 
all cases of mouth-breathing, even if the patient is addicted to 
this habit for a few hours a day only, there is very little hope 
of checking the disease ; still further, in such cases the general 
symptoms seem more pronounced. It is essential, therefore, 
to ensure proper nasal breathing. Where the patient breathes by 
the mouth the nasal cavity must be examined and any obstruc- 
tion removed. Some patients persist in the habit of mouth- 
breathing after a free nasal passage has been obtained. The 
habit can, however, often be overcome by the use of the 
apparatus suggested by Mr. W. W. James and shown in fig. 80. 



The therapeutic measures to be adopted may be divided into 
(I) Local and (II) General. 

(I) Local Treatment. 

Local treatment consists in the promoting of asepsis as far 
as practicable by securing efficient drainage. Efficient drainage 
relieves the tissues of the constant injury arising from the toxic 
matter around the teeth and the tissues react more readily. It 
may be confidently affirmed that the more thoroughly the pockets 
are kept free from sepsis, the greater will become the prospects 
of staying the progress of the disease. In theory efficient 
drainage would seem an easy matter to establish ; in practice, 
however, such is not the case. The local remedies employed 
should be directed towards — 

Fig. 80. 

(a) Freeing the teeth from salivary calculus and other debris. 

(b) Reducing the depth of the pocket. 

(c) Cleansing the pocket. 
(</) Massage of the gums. 

(a) The removal of salivary calculus allows the pockets to 
drain more freely and facilitates irrigation of the pockets. The 


scaling must be done thoroughly and special care taken to remove 
any calculus in the interstitial spaces. Where there is much- 
gingivitis it is advisable to delay the scaling until the gingivitis 
has been reduced by appropriate treatment, and the general 
resistance raised by improving the general health. The opera- 
tion of scaling can then be carried out more efficiently and 
with less laceration of the tissues. 

(b) In considering methods for reducing the depth of the 
pockets, it must be remembered that the pockets are deepest at 
the most inaccessible parts, i.e., in the interspaces. The regular 
use of astringents will often produce good results. Tannic acid 
used in the 'form of a powder may be adopted and should be 
rubbed into the gums for two minutes once a day, the treatment 
being continued for at least two months. If at the end of this 
period the gum margins have shrunk the application may be 
reduced from once a day to twice a week. As tannic acid is 
liable to leave an indelible stain on linen, patients using it should 
be warned against wiping their hands on clean linen. 

The free removal of the redundant gum with scissors and 
small knives is an excellent method of reducing the depth of 
the pocket, especially where there is considerable destruction 
of the membrane on the labial aspects. The actual cautery 
is another useful method of destroying the gum margins ; this 
method is especially useful in the interproximal spaces. 

y (c) Regular cleansing of the pockets and interproximal 
spaces by the patient is the essential part of the local treatment 
Firstly, the spaces between the teeth must be freed of food 
debris by means of " floss silk," and the gums should then be 
well squeezed between the thumb and the first ringer, with a 
downward pressure on the upper teeth and an upward pressure 
on the lower teeth. The next step is to " irrigate the pockets.'' 
If the irrigation can be easily carried out no special fluid is 
necessary and a free flushing with sterilized water would be 
effective. The most efficient method is to flush the pocket with 
peroxide of hydrogen (vols, xv), using a hypodermic syringe 
The needle of the syringe is passed well into the pocket and 
gentle pressure exerted. The use of force is to be deprecated 


as it is essential that any granulation tissue that may be present 
should not be broken down. But as a hypodermic syringe 
cannot be readily manipulated by the very large majority of 
patients it is generally necessary to try an easier, if less efficient, 
means of irrigation. I find the best plan is to have the pockets 
wiped out with a wisp of cotton-wool dipped in hydrogen 
peroxide, the cotton-wool being wound round a fine broach. 
It is necessary to give patients very precise instructions. The 
broach should be of the type ordinarily used for root canal 
dressings. The method of winding the wool on the broach 
should be demonstrated. I would suggest the following plan : 
Spread a wisp of cotton-wool along the palmar surface of the 
terminal phalanx of the first finger of the left hand ; place the 
broach on the centre of the wool ; fold the cotton-wool over the 
broach ; bring the thumb on to the broach and then run the 
thumb with the broach up the palmar aspect of the first finger ; 
the fragment of wool over the point should then be turned down 
so as to prevent the point sticking through. 

Such detailed instructions may seem hardly necessary, but 
experience has taught me that the success of this method of 
treatment depends in a large measure on the skill of the patient 
in twisting the wool on to the broach. The patient should be 
shown exactly where and how to apply the peroxide, and 
instructed to pay special attention to the irrigation of the 
spaces between the posterior teeth. The hydrogen peroxide 
to be used should be poured into a small receptacle, and any 
left unused should be thrown away and not returned to the 
bottle. The pockets should be cleansed at least once a clay, 
the best time being shortly before retiring for the night. 

If the patient will only carry out this method of cleansing 
the spaces thoroughly and regularly, a marked improvement may 
be confidently anticipated. 

(d) Massage of the gums by regular rubbing with the fingers 
and with the tooth-brush will assist in improving the condition 
of the gum margins. 


(II) General Treatment. 
General treatment consists in raising the resistance of the 
tissues and may be considered under the following headings : — 
(i) Hetero-inoculation (vaccine therapy). 

(2) Auto-inoculation. 

(3) Treatment directed towards the removal of systematic 
intoxication and a general improvement in health. 

(1) Hetero-inoculation, Vaccine Therapy. — This method of treat- 
ment aims at assisting the tissues to defend themselves against 
the action of bacteria and their products. The method of 
procedure suggested by Eyre 1 is as follows : " The patient is 
instructed to grasp the lip opposite the affected teeth with the 
forefinger and thumb of each hand and draw it away from the 
gums ; in some cases a small roll of absorbent cotton-wool is 
packed into the sulcus between the alveolar process and the lip. 
The gum margin is next wiped with a sterile swab of cotton-wool 
mounted on the end of a stick, and the gum itself dried with a 
second sterile swab. Then with another swab firm pressure is 
made on the gum over the root of the tooth. The first drop or 
two of pus that exudes is mopped' up with a third sterile swab 
and the pressure continued, and the pus that next exudes is 
collected on still another sterile swab, or by means of a stout 
platinum needle. This pus is employed for the purpose of 
making coverslip films. Finally, more pus is expressed in a 
similar way and used to inoculate tubes of nutrient media." 

The most satisfactory method is to extract a tooth when this 
is practicable, for preference a molar, and take a culture from 
the space between the roots or from near the apex of the tooth. 
Pure cultures of the various micrococci present are then obtained 
secundum artem. The patient's serum is next examined with a 
view to obtaining evidence of the presence of antibodies to some 
or any of the organisms isolated which would indicate actual 
and active infection. Opsonins, amboceptors, and agglutinins 
are the most useful antibodies in this connection, in the order 
mentioned. The organism towards which a low index (0*5 or 

1 Proc. Roy. Soc. Med. (Odont. Sect.), vol. iii, p. 34. 


lower) or a high index (1*3 or higher) is recorded is usually 
regarded as the possible origin of infection and from this 
organism a vaccine is prepared. (Mr. Goadby suggests that 
if more than one organism shows a low index a mixed vaccine 
of the several organisms should be obtained.) If two or more 
organisms are associated, as is frequently the case, a separate 
vaccine should be prepared of each, and if subsequent observa- 
tions of the index towards each bacterium are recorded, the 
dosage of either vaccine may be modified as necessary. In all 
cases, and particularly if improvement is slow, further bacterio- 
logical examination of the case should be made from time to 

The vaccines are prepared in doses of varying strength, each 
dose being placed in a small sterile glass bulb. The dose 
depends upon the responsible organism. Dr. Eyre recommends 
doses as follows for the most commonly encountered infecting 
micro-organisms : — 

Micrococcus catarrhalis if apparently the 

sole infecting organism ... 
Micrococcus catarrhalis associated wiih 

Micrococcus paralelragenus 
Micrococcus pyogenes aureus ... 
Streptococcus lanceolatus pneumonia (with 

which Streptobacillus mala (Goadby) 

is probably identicil) 
Streptococcus pyogenes longus ... 
Bacillus pneumonia (Friedlander) 
B. pyocyaneus 

The injection of the vaccine must be carried out under 
strictly aseptic precautions. 

(2) Auto-inoculation. — D. E. C. Hort ' has drawn attention 
to the fact that in vaccine therapy the damage to the tissues by 
the toxic products of autolysis and other cell metabolism is not 
taken into consideration. These toxic products are combated 
by the formation of corresponding antibodies. Any method of 
treatment which produces hyperemia in the part, whether by 
the use of poultices or blisters or Bier's treatment, acts by 

1 Proc. Roy. Soc. Med. (Med. Sect.), vol. ii, No. 6. 

5 ■ 


.. 25 . 

• • 50 


.. 25 . 

.. 50 . 

■■ 75 


.. 25 . 

.. 50 

5° • 

.. 100 

.. 250 

.. 500 

5 • 


.. 25 . 

.. 50 

S ■ 

.. 10 

.. 25 

.. 50 

5 ■ 


.. 50 . 

.. 100 

10 . 

• • 5° • 

.. 100 

.. 250 


increasing the fluid exudate in the affected parts; in this way 
the irritant is diluted and the natural antibodies increased in the 
area ; in other words, the treatment may be regarded as a 
process of auto-inoculation. 

The ideal method of producing hyperaemia would seem to 
be that suggested by Dr. Bier, but it presents some practical 
difficulties. To carry out the treatment a splint is made to grasp 
the gums as high above the teeth as possible (fig. 81). The 
spring should be so adjusted as to cause sufficient pressure to 
congest the gums without causing pain. The splint should be 
applied for about fifteen minutes twice a day. 

Fig. Si. — Semi-diagramatic view of splint. 

A useful apparatus for producing hyperaemia of the gums has 
been suggested by Mr. H. Woodruff. A vulcanite cap is made 
to grasp the margin of the gums as high above the tooth as 
possible, the remaining portion of the cap being made so that 
a slight space exists between the gums and the splint. A tube is 
inserted into the splint and connected with an exhaust bulb. 
The apparatus is shown in fig. 82. The cap is placed over the 
teeth and the air is gradually exhausted. By this means an 
effective hyperaemia is obtained. From a practical point of view 
the results from this line of treatment have been disappointing. 

The nearer the health approaches to the normal standard the 
greater becomes the resistance of the tissues and their power to 
react. An impairment of the general health means a lowering 
of the resistance of the tissues and of their power to react ; it is, 
therefore, very important that steps should be taken to improve 
the general health as far as possible. This part of the treatment, 

8 4 


however, belongs to the province of the general medical 

The question of treatment must now be considered more in 
detail, and it will be convenient to discuss separately the cases 
which are favourable for treatment and those which are not. 

Fig. 82. 

(1) Cases favourable for Treatment. 

A case may be regarded as favourable for treatment if the 
following conditions are found : — 

(a) The pockets around the teeth are shallow. 

(b) The arch is well developed, and the function of mastica- 
tion is efficiently performed. 

(c ) There are indications of recuperative powers on the part 
of the patient. 

(d) The patient is a nose-breather. 

As the pockets, which are the real cause of the trouble, 
cannot be removed, treatment resolves itself into a question of 
drainage. The more thoroughly the pockets are cleansed, the 


greater will be the chance of staying the progress of the disease. 
The teeth must be thoroughly scaled, and the patient instructed 
to carry out the following daily routine: — 

(a) Pass silk between the teeth to free the spaces of food 

(6) Squeeze the gums so as to expel as much material as 
possible from the pockets. 

(c) Brush the teeth and gums thoroughly with a stiff brush. 

(d) Irrigate each space with peroxide of hydrogen, as 
suggested on p. 79. 

{e) Twice a week apply to the pockets a 2 per cent, solution 
of iodine in alcohol. 

These simple measures, if faithfully carried out, will suffice 
to arrest the disease in favourable cases. I have tried raising the 
resistance of the tissues by means of vaccines and Bier's method 
of congestion, but I am not satisfied that these cases showed 
greater improvement than others where the treatment was limited 
to irrigation. 

Thorough cleanliness of the "pockets" is the keynote in 
treatment, and if this is achieved an arrest in the progress of 
the disease may be expected. The following cases may be 
quoted as examples : — 

M. B. This patient, a well-developed female, was seen early 
in 1910. A well-marked gingivitis was present, with a slight 
thickening of the alveolar process, shallow pockets around the 
teeth, and a fair degree of attrition of the teeth. 

The patient was a nose-breather. She was suffering from 
indigestion and rheumatism. Local treatment on the lines 
indicated above was adopted. The patient has lost all her 
general symptoms, and her mouth is healthy. Skiagrams taken 
before and after treatment show that in this case the condition 
of the bone is stationary (figs. 83 and 84). 

This patient was last seen in October, 191 5. She was still 
carrying out the treatment, and the condition of the alveolar 
process was practically similar to that shown in the diagram 
taken in October, 191 1. 

F. S. This patient was a female, well developed, and was first 



seen in the latter part of 1909. The gums were as shown in 
fig. 85. There was marked gingivitis, but no apparent general 
symptoms. Skiagrams showed a fair amount of bone destruc- 
tion. The patient was a partial mouth-breather, breathing by 
the mouth during sleep. Vaccines were tried without any 







Fi«. ;83- — The light appearance of the film taken in February, 1910, is due to 








Fir. 84. 

irrigation of the tooth pockets. The condition showed no 
improvement, the discharge continuing from the gum margin. 
Local measures on the lines suggested were adopted, and the 
patient has very faithfully carried out her part of the contract. 


Fig. 85. 

Fig. 86. — Skiagrams: {a) taken December, 1909; (i) November, 1911. 


In this case the disease is progressing very slightly. Skiagrams 
taken at the commencement of treatment, and in November, 
191 1, are shown in fig. 86. 

When last seen the disease was slowly progressing in spite 
of regular treatment carried out by the patient. The continued 
progress is to be attributed to the fact that the patient is a partial 

H. J. This patient came under treatment in December, 
1908, suffering from suppuration in the left antrum and marked 
periodontal disease. The antrum was opened on December 23, 
and treated by lavage. Rapid improvement followed, but the 
discharge did not wholly clear up. A vaccine of Staphylococcus 
albns was used, and this treatment appeared to arrest the antral 
suppuration completely. A slight mucoid discharge occasionally 
appears, and the patient prefers to undertake the regular irriga- 
tion of the antrum rather than submit to a more extensive 
operation via the nasal fossa. 

The periodontal condition was treated by scaling and irriga- 
tion of the tooth pockets. Bier's treatment was adopted for the 
anterior upper and lower teeth, the splints being used twice daily 
fifteen minutes at a time. At the end of 1909 the gum condition 
had considerably improved, and the patient's weight increased 
from 10 st. 2 lb. to 11 st. 12 lb. 

Since then the treatment has been continued at intervals. 
Skiagrams show that the periodontal disease is practically 

(2) Cases not favourable for Treatment. 

Cases which are not favourable for treatment are those show- 
ing well-marked signs of rarefying osteitis and with general and 
local conditions, which indicate that the tissues have little re- 
cuperative power ; also all cases of persistent mouth-breathing. 
It will be convenient to group these cases under two separate 
headings, viz. : (a) Cases unassociated with apparent symptoms ; 
and (b) cases in which a causal relationship to other diseases 
has been established. 


(a) Cases Unassociated with Apparent Symptoms. 

As regards cases falling under this heading, there are certain 
points which must be kept clearly in mind in endeavouring to 
arrive at the right line of treatment. Although efficient irrigation 
may check the discharge from the tissues, and some advantage 
may be gained in an attempt to raise the resistance of the tissues 
by the aid of auto- or hetero-inoculation, all such efforts will fail 
to stop the advance of the disease. Under these circumstances 
the question arises whether it is justifiable to continue a course 
of treatment which, at the best, can do no more than slow down 
the progress of the disease. My own view is that such a course 
of treatment cannot be justified for two reasons : (1) Because a 
potential source of infection remains which may become active 
at any moment, and (2) because the destruction of the alveolar 
process is proceeding and thus increasing the difficulty of pro- 
viding artificial dentures which will be efficient and comfortable. 

The following case illustrates the first point : — 

F. O., a female, aged 27, was first seen in July, 1909, and 
came under treatment on account of looseness of the teeth. 
Beyond slight indigestion she appeared to be in good health. 
The patient was a mouth-breather. A blood count taken showed 
a normal condition. The skiagrams indicated considerable 
rarefying osteitis (see fig. 87). 

Extraction was advised, but was deferred at the earnest 
request of the patient, and an endeavour made to treat the con- 
dition locally. Three teeth were removed and local treatment 
and vaccines were tried. When seen in October, 19 10, the 
condition of the mouth had improved and the teeth were firmer. 
The patient did not return again until February, 191 1, and stated 
that she " had got tired of local treatment." Her condition was 
as follows : The skin was blotchy ; her periods were irregular ; 
she was suffering from gastritis, and complained of feeling 
thoroughly ill. A blood count showed well-marked anaemia and 
leucocytosis. The following teeth were removed : — 

654321 I 12345 

8 4321I12345 8 



The patient recovered completely. This case is typical of 
many met with in practice. Local treatment is carried out at 
first, but is dropped gradually, and the mouth condition becomes 
an active focus of infection. 

The second reason for early removal of the teeth in cases 
where the disease is making progress is also of practical import- 
ance. The progress of the disease implies destruction of the 
alveolar process, and eventually results in the complete disap- 
pearance of the alveoiar process. From the prosthetic aspect it 
is then necessary to deal with a mouth devoid of ridges on which 
dentures can be steadied. Such cases are obviously unsatis- 












Fig. 87. 

factory both to the practitioner and to the patient. If the teeth 
are removed at an earlier stage while there is ample alveolar 
process on which to rest the denture, the insertion of the denture 
will restore function to the bone, and, in most cases, a well- 
marked ridge will remain permanently. 

For the foregoing reasons I have no hesitation in advising the 
rt-moval of the teeth. 

The following case is extremely interesting in its bearing on 
this problem. The models marked (a) in figs. 88 and 89 were 


9 1 

taken at the age of 40, and those marked (6) at the age of 75. 
The history of the case is briefly this : The premolars and molars 
had become loose and had fallen out, and as there was nothing 
to be gained by retaining the remaining teeth — sixteen in all — 
they were removed, dentures being inserted. If the models are 
carefully examined, it will be noticed that, where the teeth were 



lost by the natural cure of the disease, the alveolar process has 
disappeared, but where the teeth were removed by extraction 
a well-marked ridge still exists. The early removal of the teeth 
resulted in the patient having for thirty-five years not only 
a clean mouth, but also dentures which have been steady and 


(b) Cases in which a Causal Relationship to other Diseases has 

been established. 

In this class of cases it is absolutely necessary that the dental 
sepsis should be completely removed. After reviewing the cases 
which have come under my notice during the last ten years, and 
careful consideration of the results of different methods of treat- 
ment, I am driven to the conclusion that the removal of the 
affected teeth at the earliest opportunity is the right course to 
adopt, and that any other line of treatment is unsatisfactory. A 
typical example of this class of case is as follows : A young 
adult is suffering from rheumatoid arthritis, and the mouth 
shows signs of general periodontal disease accompanied by 
rarefying osteitis in a marked degree. The case is one in which 
the potential source of trouble — that is, the pockets — cannot be 
removed by treatment. The choice here lies between retaining 
the teeth and running serious risk of an aggravated arthritic 
condition on the one hand, or, on the other hand, removing 
the teeth and ensuring useful joints. In my opinion, the latter 
course alone can be justified, as artificial dentures can be 
provided, but not new movable joints. 

In carrying out extraction in these cases the following 
course is adopted : The mouth is made as healthy as possible 
by thorough irrigation of the pockets with hydrogen peroxide. 
The premolars and molars are next removed and the mouth 
is allowed to heal. Models of the mouth are then taken with 
the incisors in place, and bites are obtained. The advantage of 
proceeding on these lines is that you avoid the difficulty which 
would be experienced in gauging the correct height of the bite 
after the removal of the front teeth. The anterior teeth are 
then removed and dentures inserted as soon as possible. The 
number of teeth which can safely be removed at one sitting 
depends largely upon the individual case. Where the " power 
of repair " is at a low ebb the extractions must be carried out by 
easy stages, but where there is ample "power of repair" the 
extractions may be carried out more expeditiously. I incline to 
the view that extensive extractions at one sitting should be 



avoided unless there are special reasons for adopting that course. 
It is said that trouble in the bone is likely to follow extensive 
extractions in these cases unless the resistance of the tissues is 
first raised by a course of vaccine treatment, but that is not my 
experience. I am disposed to think that, where trouble in the 
bone occurs as a result of extractions, it is almost always due to 
the damage inflicted on the tissues by the operation. A rise in 
temperature seldom follows the extractions if the mouth is kept 
clean. Occasionally a rise in temperature does occur, as is well 
shown in fig. 90. In that case the patient was suffering from 
a corneal ulcer, and the removal of each batch of teeth was 
followed by a rise in temperature. 

AUG. 1911 SEP 

DATE 31 1 2 3 4 5 

6 7 8 9 10 11 12 

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Fig. 90. 

In cases where general trouble is traceable to the mouth it 
has been my practice to retain the anterior teeth, provided that 
the bone destruction is slight. The argument in favour of 
retaining the teeth in these cases is that the pockets around the 
anterior teeth are easily accessible and can be thoroughly irri- 
gated by the patient. Experience of these cases has taught me, 
however, that if the patients are mouth-breathers it is only a 
matter of time before extraction becomes imperative. In this 
connection the following case is instructive. The premolars 


and molars are removed for a patient suffering from naso- 
pharyngeal trouble. The remaining teeth were faithfully treated 
by the patient and the gums appeared to be in a fairly normal 
condition. At the end of four years, notwithstanding the care 
bestowed on the teeth by the patient, the bone destruction was 
progressing rapidly and there was a large amount of trouble 
around the teeth, necessitating their removal. Would it not 
have been a sounder policy, and much safer, if these teeth had 
been removed when the original extractions were carried out ? 

I am well aware that treatment by free extraction of all teeth 
which are the source of sepsis, as suggested above, is opposed 
to the teachings of many practitioners. With those who hold 
that local treatment will often result in a disappearance or at 
least an improvement in the general condition I fully agree, but 
— and this is the important fact — the source of sepsis has not 
been eradicated. The sepsis may possibly be lessened in degree, 
but nevertheless it remains and must continue to damage the 
tissues slowly but surely. The damage to the tissues is progres- 
sive, and when, through the loss of the teeth, a natural cure of 
the teeth is effected, the damage of the tissues may be irreparable. 
Dental practitioners cannot be justified in allowing such a con- 
dition to be brought about, and it is our duty to place clearly 
before the patient the risks they run. 

Let us take as an example a patient who has been attacked 
for the first time with rheumatoid arthritis (polyarthritis), the 
toxic origin of which has been traced to the teeth. Here the 
following considerations should influence our decision as to 
advising free removal of the teeth : — 

(i) Each fresh attack increases the injury to the joints and 
lowers the power of reaction of the tissues. 

(2) Every tooth with a marginal gingivitis is a potential 
source of infection. 

(3) The absorption of the toxins in these cases is often via 
the bone, skiagrams usually showing a fair amount of rarefying 

(4) Vaccine, ionic medication and local measures do not 
remove the real cause, namely, the pockets around the teeth, 


and the patient, even if the condition has improved, is still left 
with potential sources of disease which may at any time set up. 
a fresh attack of arthritis. 

(5) The results following complete removal of the teeth are 
permanent, providing there are no other sources of infection. 

Having discussed from a general point of view the treatment 
of periodontal disease, we may with advantage consider the 
important question of the value of vaccines. 

Vaccine therapy aims at assisting the tissues to defend them- 
selves against the action of bacteria and their products. It is 
essential for success, therefore, that we should know the 
causative organism of the disease which has to be treated. 
There is reason to believe, however, that periodontal disease is 
not caused by any special organism ; but even if it is due to a 
specific organism, that organism has not yet been identified. In 
the treatment of periodontal disease vaccine therapy therefore 
fails to satisfy the most important requirement. It may be urged 
in favour of vaccine treatment that the infection in the pockets 
is causing local injury, and that vaccines will check the injury 
by raising the resistance of the tissues in the neighbourhood of 
the tooth. The difficulty here lies in the fact that the infection 
is invariably mixed, and the vaccine therapist must needs prepare 
a vaccine of all the organisms found. The practice, however, 
is to use a vaccine of the predominant organism or perhaps of 
two of them, and, under these conditions, the treatment is 
necessarily incomplete. But, granting that vaccine treatment is 
occasionally successful, the pockets still remain, and no amount 
of vaccine treatment will remove them. 

Apart, however, from any considerations which may be 
regarded as more or less theoretical, the question arises whether 
vaccines lead to good results in the treatment of periodontal 
disease. I have had personal experience of nearly forty cases 
of periodontal disease which were treated with vaccines, and in 
no single case was a cure effected and in only a few cases could 
I detect any improvement. 

When vaccine treatment is carried out concurrently with 
local remedies and improvement results, it is extremely difficult 


adequately to assess the amount of improvement which should 
be ascribed to the local measures on the one hand and to the 
vaccines on the other. It is the general experience that the 
majority of cases treated with energetic local measures will show 
a rapid improvement. 

In papers advocating the treatment of periodontal disease by 
vaccines, one constantly reads that a large percentage of the 
cases are labelled as cured. Manifestly much depends upon the 
exact meaning placed by the practitioner on the word "cured," 
and reference to this point has already been made (see p. 77). 
Eyre and Payne 1 do not take the view there expressed, but class 
as "cured'' all cases where "the affected teeth are firm so that 
mastication is painless and the mouth comfortable, no pus can 
be expressed from the sockets, the pains and other symptoms of 
ill-health have disappeared, and the patient feels ' quite well.' " 

In such cases the patients are, in mv opinion, relieved only 
and not cured, and to lead them to think that they are cured is 
to invite them into a "fool's paradise." The pockets remain and 
recurrence of trouble is only a matter of time. 

In the treatment of the general condition arising from mouth 
infection vaccines may undoubtedly be extremely useful. The 
following case illustrates the occasional value of vaccines in the 
treatment of diseases which owe their origin to mouth infection: 

A patient, aged 36, was seen on January 27, 19 13. He 
was a carpenter's labourer, and since August 191 2 had been 
under treatment for iritis in the right eye. There was no history 
of syphilis. The incisors and first molars were hypoplastic and 
there was very marked periodontal disease. He weighed ten 
stone. The following teeth were removed : — 

54321 1 1 2 3 4 67 
87 54321 I 1234567 

By the middle of February all the teeth had been removed and 
a culture of streptococcus was obtained from the discharge 
between one of the maxillary molars. A vaccine was prepared, 

1 Proc. Roy. Soc. Med. (Odont. Sect.), vol. iii, p. 39. 


but, owing to the fact that the patient was undergoing tuberculin 
treatment, it was not used until the end of April. The eye 
lesion, although slightly better, did not clear up with the 
tuberculin injection and it was not until streptococcal vaccine 
was used that any marked improvement was noticeable. The 
vaccines were stopped early in June when the eye condition 
showed considerable improvement. The patient was again seen 
in October. He had gained nearly one stone in weight, the 
inflammatory trouble had cleared up, but unfortunately the 
sight of the eye had been lost. The points to be noted in this 
case are : — 

(1) There was no improvement in the eye condition under 
local remedies. 

(2) The removal of the teeth, although improving the general 
condition of the patient, did not lead to any definite improve- 
ment in the eye condition. 

(3) There was no apparent improvement with the tuberculin. 

(4) Rapid improvement followed the use of the streptococcal 

The inferences to be drawn from these facts are that the eye 
lesion was due to infection in the mouth, and that, although 
removal of the teeth cut off the source of sepsis, the reactive 
powers of the patient were insufficient to cope with the eye 
infection until assisted by the vaccine. 

The case shows the occasional therapeutical value of 
vaccines for treating lesions started by septic foci in the mouth, 
but the vaccine in this case would have proved of little value 
if the septic focus had been allowed to remain. It is highly 
probable that if the teeth had been removed as soon as the eye 
lesion was recognized the sight of the eye would have been 

Ionic medication is claimed by many practitioners to be of 
great value in the treatment of periodontal disease. My colleague, 
Mr. Norman Bennett, for whose opinion I have a great respect, 
has kindly contributed the following notes on this method of 

98 chronic general periodontitis 

Electro-therapeutic Treatment. 

Basis of Therapeutic Action, — Electro-therapeutic treatment of 
periodontal disease depends upon the processes of cataphoresis 
and ionization separately or jointly. An electric current passed 
through a tissue or other substance has the power of trans- 
porting liquids, which may contain substances in solution, in 
the direction of the flow of current. The direction is from the 
positive to the negative pole, from the higher potential to the 
lower. In this way the tissue in the vicinity of the pole may be 
penetrated by an antiseptic drug to an extent impossible with 
mere application. This process is called cataphoresis. Another 
and probably more important effect of the passage of current 
therapeutically is the power of decomposing substances con- 
tained in solution, the " ions '' migrating in opposite directions 
towards the positive and negative poles ; penetration is thus 
produced as in cataphoresis, but instead of a soluble salt being 
forced unchanged into the tissues, the nascent metallic elements 
freshly liberated from their soluble salts are so used. This 
process is called ionization. It is exactly the same as the familiar 
process of gold-plating, in which a positive electrode of gold, a 
negative electrode of the article to be plated, such as German 
silver, and an electrolyte of gold cyanide are used ; the gold salt 
is decomposed, the gold passes towards the negative pole and 
is there deposited, and the cyanogen reacts with the gold 
electrode and forms fresh cyanide, which goes into solution. 
Certain elements such as zinc, copper, silver (in fact, most of the 
metals), are called electro-positive, because they migrate from 
the positive to the negative pole. Most of the non-metallic 
elements, such as oxygen, chlorine, iodine, pass in the reverse 
direction, and are therefore called electro-negative. In the 
usual application of the electric current to the body in 
conjunction with a metallic salt, probably the two processes 
of cataphoresis and ionization occur coincidently. 

Apparatus. — The current used is a weak constant current. 
Readers who desire a detailed description of apparatus should 
consult special works, but it may be well here to give a brief 




description of the essential parts. The current may be obtained 
from the main (from dynamos) or from a battery of cells. In 
the former case resistance must be inserted to reduce the current 
to a low voltage, and certain precautions must be taken to 
insulate the chair from earth and the patient from his sur- 
roundings. A battery is equally convenient and absolutely safe, 
and is preferred by the writer. It should consist of a sufficient 
number of Leclanche or dry cells to give a maximum voltage 
of not more than forty volts. A current of this strength is too 
great for most purposes ; it is therefore necessary to use a 
rheostat in circuit, so that a current of very low electro-motive 
force may be applied in the first instance and afterwards 
increased. A milliampere-meter should also be used in circuit, 
as it is necessary to know always what strength of current is 
being used. The active electrode may consist of a piece of 
platinum, zinc, or copper, flattened to form a small blunt 
spear-head point, and slightly curved. A convenient form for 
the indifferent electrode is a metal cylinder, which should be 
wrapped round with a thoroughly damp cloth and held in the 
patient's hand. 

Technique. — ■ It is of course to be presumed that before 
treatment is commenced calculus has been removed and the 
mouth generally got into as clean and healthy a condition as 
possible. It is not necessary, or in many cases possible, to 
remove all calculus as a preliminary to treatment ; the process 
can be better completed during the course of treatment ; indeed 
small areas of marginal gingivitis that do not respond will 
often be found to be covering a small deposit of undiscovered 

The drug that the writer has found most useful is a 
5 per cent, aqueous solution of zinc choride ; but salts of 
copper, such as the sulphate, or of silver, may be used. 

A few contiguous teeth should be isolated and kept 
moderately dry by means of napkins, wool-rolls, or bibulous 
paper. Absolute dryness is not necessary, but too much 
moisture will not only dilute the drug unduly but also allow 
the current to pass superficially instead of through the tissues. 


The current having been turned on and the rheostat control 
advanced a short distance, the electrode, previously wrapped 
round with a small quantity of cotton-wool, should be dipped 
in the solution and applied to the gum at least a quarter of an 
inch from the neck of a tooth ; it should then be slid carefully 
over the gum until the neck of the tooth is reached and passed 
down into the pocket round the tooth. The most important 
parts are the approximal pockets. It is usually convenient to 
treat about half a dozen teeth at a time, dealing first with the 
labial or buccal aspects and the approximal pockets, and 
completing on the lingual aspect. The amount of current 
registered with any given voltage varies inversely with the 
resistance of the body. This resistance itself varies with 
different patients and with the same person at different times. 
The amount of current that can be tolerated is usually from 
one to five milliamperes. It will usually be found that a current 
of one milliampere is not felt at all ; more than live cannot 
usually be borne, except perhaps in the molar region. A 
current of three milliamperes is usually sufficient for therapeutic 
effect, and tolerable to the patient. Of course, the character 
of the patient and of the teeth are determining factors. 

A current of low electro-motive force having been tried at 
the outset, it can be gradually raised by moving the rheostat 
control until sufficient is obtained. It should be remembered 
that most pain will be felt when the needle is first applied (the 
" make " of the current), less when it is broken, and least Of 
all during the passage of the current, so long as the electrode 
is stationary. That is why the needle should, every time it has 
been dipped in the solution, be first applied to the gums and 
then moved to the tooth. If a large drop of liquid is hanging 
on the needle a considerable amount of pain may be felt at 
the first contact. Care should be taken to move the needle 
smoothly from one tooth to the next without making contact 
or even altering the area of contact more than necessary, 
because the current is felt more severely when passed through 
a small area than a large. When the teeth are very sensitive it 
is sometimes necessary to apply the needle first and then 


gradually turn the current on from zero ; in this way pain may 
be greatly minimized. 

By taking' groups of teeth in succession the whole mouth may 
be treated in about three-quarters of an hour, but it is often 
desirable to spend the greater part of the time over the most 
seriously affected teeth, three or four minutes being devoted to a 
single tooth. The only visible sign noticeable is a slight whiten- 
ing of the edge of the gum, and a kind of white deposit spread- 
ing from the edge. It is only very rarely that any sensation is 
felt in the hand of the patient holding the negative electrode. It 
is, however, desirable that rings should be removed. 

The application should be repeated every second or third day 
for a fortnight, then less frequently until about ten or a dozen 
applications extending over five or six weeks have been made. 
In this period it will be possible to judge results, and if consider- 
able improvement cannot be obtained in that time or even less, 
it is not likely to be gained at all. 

Efficiency of the Method. — In discussing the efficiency of 
ionization it is necessary to have clearly in mind what is being 
attempted. In the opinion of the writer there are in most cases 
of periodontal disease a constitutional factor and a local factor, 
the latter being a bacterial infection of the pockets, the gum 
margin, and the alveolus. In some cases the former pre- 
dominates, and in others the latter. Inasmuch as the rationale 
of the treatment consists mainly in a more perfect sterilization of 
the pockets than can be obtained in other ways, it is obviously 
in the infective cases that it will be likely to be most useful, and 
especially in early cases. On the other hand, a large number of 
cases of periodontal disease exhibit as their cardinal features a 
clean mouth, no marginal gingivitis, anaemic gums, considerable 
absorption of bone, and only shallow pockets, because the gums 
have receded pari passu with the absorption of bone. These are 
the cases that are thought usually to be associated with absorp- 
tion of bacterial products into the blood-stream, rather than by 
the intestinal tract, as when there is a marked flow of pus from the 
pockets : they are the cases generally connected with arthritic affec- 
tions. In these patients it cannot be expected that a sterilizing 


effect will be so valuable. Tbe writer believes, however, that 
the treatment is beneficial. It is more than likely that the 
current has a stimulating effect on the metabolism of the tissues, 
and there is also a secondary result that is much appreciated by 
patients. It is well known that in the kind of case now being 
considered far more pain and discomfort are occasioned by the 
disease than in the more septic cases. The necks of the teeth 
become acutely tender, so that meals become a source of misery. 
The writer has satisfied himself that if a current of low electro- 
motive force is used for the first few sittings and gradually 
increased, this sensitiveness can be much reduced and even 
abolished, and that in some cases the cure remains good for a 
very long time. 

In the class of cases first referred to — thos^ in which there is 
marked gingivitis, deep pockets, and much pus — it is obvious 
that the treatment cannot be expected to produce infallibly a 
permanent cure. The pockets may be sterilized, but will probably 
become reinfected, and the whole train of consequences will be 
reproduced unless further steps are taken. 

In early cases the writer considers that ionization affords the 
best means of sterilizing the gum margins and shallow pockets, 
and if accompanied and followed by reasonable prophylactic 
measures on the part of the patient effects a practical cure. 




Adami, process of intestinal toxnemia, 66 
Adventitious tissue, masses of, in cleft 

between roots of molars in peri- 
odontal disease, 15 
Aged, the, gastric ulcer in, connection 

with oral sepsis, 69 
Alimentary canal, abnormal conditions 

of, 66 
, bacteria of, toxic products, how 

neutralized, 65, 66 

, normal condition of, 64 

Alveolar plate, outer, rarefying osteitis 

of, rare in herbivora, 20 
— process, destruction in periodontal 

disease, 5. 6 

, early affection of, 61 

, effect of well-performed mastica- 
tion on, 61 
, formation of nodular masses of 

bone on outside of, II, 12 
, gradual disappearance with ad- 
vancing age, 2 

, normal, 1, 2 

, retention and preservation of, 

aided by early extraction of teeth in 

periodontal disease, 90, 91 
, necessary for satisfactory 6t- 

ting of dentures, 90, 91 
, skiagrams in individual, with 

normal gums, 2, 3 
Amoebae, association with pyorrhoea 

alveolaris, 51 
Andrewes, F. \V., fate of toxic products 

of bacteria of alimentary canal, 65. 

Animals, periodontal disease in, 16 
Anhritis, multiple, teeth from case of 

periodontal disease associated with, 

14, 15 

Arthritis, rheumatoid, complicating peri- 
odontal disease, 73 

■ , extraction of teeth in, 

92, 94 

, reasons for, 94 

Astringents in reduction of pockets, 79 
Auto-inoculation in periodontal disease, 


Bacillus prodigiosus, self-infection of 
mouth with, to determine time of 
stay of organism in mouth, 65 

Bacteria from mouth, fate of, in stomach, 

— , inhibition by gastric juice, 69 
— , multiplication in intestines, 65 
— of alimentary canal, toxic product?, 

how neutralized, 65, 66 
— , toxic products of, absorption into 

general circulation in periodontal 

disease, 66, 67 
Bacteriology of periodontal disease, 4$- 

Battery for use in electro-therapeutic 

treatment of periodontal disease, 99 
Bear, spectacled (Ursus ornatus), skull 

showing periodontal disease, prob- 
ably from injury to right maxillary 

canine, 22, 23 
Bennett, Norman, electro-therapeutic 

treatment of periodontal disease, 97 
Bier's method in periodontal disease, 

55, 57, 83, 85, 88 

, splint for, 83 

Black, function of gingival organ, 59 
Bone, destruction of, in chronic general 

periodontitis, maxilla showing, 3, 4, 5 
, most marked on anterior aspects 

of teeth, II, 12 
— ■ in mandible, skiagrams showing 

appearance of, I, 2 



Bone, rarefaction of, in periodontal 
disease, 9, 10 

, limitation of, 10 

— , thickening of margin in very chronic 
case of periodontal disease, 10, 11 
- tissues surrounding teeth, growth of, 
on what dependent, 61 

Breath, sickly sour odour of, in peri- 
odontal disease, 38, 39 

Brewers' slops, cows fed on, liability to 
interstitial gingivitis, 49 

Bull-dogs, periodontal disease in. 48 


Calculus, deposit around teeth, cause 
of, 59, 60 

— , salivary, removal in periodontal 
disease, 78 

Cammidge's pancreatic reaction in jaun- 
dice, 70 

Canine tooth, right maxillary, probable 
injury to, setting up periodontal 
disease in bear, 22, 23 

Caries and periodontal disease, difference 
between, 63 

Cataphoresis in electro-therapeutic treat- 
ment of periodontal disease, 98 

Cataract, senile, operation for, in case 
of periodontal disease, 76 

Cats, destruction of tissues forming tooth- 
socket in, 47 

— , marginal gingivitis in, 47 

— , periodontal disease in, 47 

, attacks highly bred animals by 

preference, 47 

— — — , due to lodgment of food 
debris, 47, 48 

Cattle, cause of periodontal disease in, 
48, 49, 62 

— , American, cause of periodontal disease 
in, 48, 49, 62 

Cautery, actual, in destruction of gum 
margins, 79 

ChafT, eating of, connection with peri- 
odontal disease in horses, 62 

Choroiditis, central, and periodontal 
disease, 74, 75 

— , disseminated, and periodontal disease, 
74. 75 

Circulation, general, absorption of toxic 
products of bacteria into, in peri- 
odontal disease, 66, 67 

Colyer, Stanley, variation in disease, 67 

Copper, salts of, in electrical treatment 
of periodontal disease, 99 

Cows fed on brewers' slop, liability to 
interstitial gingivitis, 49 


Daniel, P., infection of lower part of 

ileum in oral sepsis, 70 
Deer, Schomburgk's ( Cervus schomburgki) 

advanced periodontal disease in, 21 
— , skull of, showing suppuration of body 

of mandible from periodontal disease, 

Dentures, satisfactory fitting of, after 

removal of teeth for periodontal 

disease, condition necessary for, 

90, 91 
Diet, modern, articles of, rarely bring 

functional activity of teeth into 

play, 61 
Disease, variation in, explained, 67 
Dogs, periodontal disease in, 24, 47, 48 
— — — , due to lodgment of food 

debris, 48 
— , long-muzzled, periodontal disease in, 

starting point, 25 
— , short-muzzled, periodontal disease in, 

starting point, 24, 25 
Domestic animals, periodontal disease 

in, 24, 47 
Drainage, efficient, in periodontal 

disease, 78 
Drugs suitable in electro-therapeutic 

treatment of periodontal disease, 99 
Duodenitis, how resulting, 70 
Dyspepsia complicating periodontal 

disease, 43 


Electrodes for use in electro-thera- 
peutic treatment of periodontal 
disease, 99 

Electro-therapeutic treatment of peri- 
odontal disease, 97-102 

, apparatus, 98 

— — , application of current, 100 

, basis of action, 97, 98 

, efficiency of method, 101 

, number of teeth to be treated 

at a sitting, 100 

, technique, 99 

Endamaba buccalis as cause of peri- 
odontal disease, 51 

, points for and against, 52 

, characters of, 51 

, stages of, 50 



Episcleritis and periodontal disease, 74 

Epithelial layer, destruction of, in peri- 
odontal disease, 31, 32 

Eye, diseases of, due to periodontal 
disease, 73, 74 

Eyre, preparation of vaccines for use in 
periodontal disease, 82 

— and Payne, micro-organisms causing 

periodontal disease, 50 


Fibrous connective tissue, transforma- 
tion of tooth-socket into, 32, 33, 
36, 37 

Food debris accumulating in pockets 
around teeth, 38, 39, 52 

, removal of, 52 

, lodgment of, producing periodontal 

disease in cats and dogs, 47, 48 

— packing, effect on tissues in peri- 

odontal disease in horse, 27, 28 
— , soft, prepared, favours onset of peri- 
odontal disease, 63 


Gastric juice, inhibition of bacteria by, 
65, 69 

Gastritis, chronic, and oral sepsis, con- 
nection between, 68, 69 

— ^following periodontal disease, 66 

— leading to inflammation and infection 

of intestinal canal, 70 

Gastro-intestinal disease due to peri- 
odontal disease, age of onset, 70 

Gingival organ, function of, 59 

— space, 3, 4 

Gingivitis in mouth-breathers cannot be 
removed by care and cleanliness, 57 

— in periodontal disease, 38, 39 

— , interstitial, cows fed on brewers' 

slop liable to, 49 
— , liability of mouth-breathers to, 39 
— , marginal, cause of, 53 
, deposit of calculus around teeth 

resulting from, 60 

, in cats, 47 

, in mouth-breathers, 52, 53 

— — , in periodontal disease, 41, 43 
, micro-organisms found in cultures 

from, 50 
— , reduction of, to precede scaling, 78 
— , spread of, arrest, 39 
Glossitis, chronic, association with 

periodontal disease, 68 

Glossitis, chronic, developing in syphili- 

tics with dental sepsis, 68 
— , superficial, in periodontal disease, 39 
Goadby, K. W. , vaccine treatment of 

periodontal disease, 82 
Gout essentially a non-suppurative 

disease, 60 
Gouty periodontitis, so-called, 60 
Gros, early observation of amcebre in 

mouth, 51 
Gum margins, destruction of, by actual 

cautery, 79 
— , redundant, free removal of, in reduc- 
tion of pockets, 79 
Gums, hemorrhage from, recurrent, in 

periodontal disease, 39 
— , hyperemia of, method for producing, 

— , normal, skiagram of alveolar process 

in individual with, 2, 3 
— , recession of, in periodontal disease, 38 


HEMORRHAGE, recurrent, from gums in 
periodontal disease, 39 

Heart symptoms, connection with peri- 
odontal disease, 73 

Herbivora, periodontal disease common 
in, 20 

— , rarefying osteitis of outer alveolar 
plate rare in, 20 

Hotdeum jubatum, penetration of mouth 
tissues of American cattle, result, 
49. 62 

Horse, periodontal disease in, 25-30, 46 

, advanced stage, 29, 30 

, cause of, 62 

, effect of food packing on 

tissues, 27, 28, 46 

, progressive stages of, 25-28, 46 

Hort, E. C., value of auto-inoculation, 82 

Hunter, W., gastritis due to oral sepsis, 69 

Hydrogen, peroxide of, flushing with, in 
cleansing of pockets, 79 

, method of application by 

patients, 80 

Hyperemia of gums, apparatus for pro- 
ducing, 83 


Ileum, lower part, chronic infection in 
oral sepsis, 70 

Ill-health, chronic, cause of, 71 

Incisors, periodontal disease commencing 
around, 5, 6 



Intestinal canal, inflammation and in- 
fection of, due to gastritis, 70 
Intestines, multiplication of bacteria in, 


Ionization in electro-therapeutic treat- 
ment of periodontal disease, 98 

— in sterilization of pockets in peri- 
odontal disease, 101, 102 

Iritis complicating periodontal disease, 
74, 76 

, treatment by vaccine therapy, 

96, 97 


James, W. \\\, apparatus for promotion 
of nasal breathing, 77, 78 

Jaundice, pancreatic reaction in, 70 

— , pancreatitis leading to, 70 


Kangaroo, skull and mandible of, 

showing advanced periodontal 

disease, 19 
— , brush-tailed (Petrogale penicellata), 

skull showing periodontal disease, 

17, 18 
Kerato-iritis and periodontal disease, 75 

Lang, \\\, eye diseases due to peri- 
odontal disease, 73 

Lap-dogs, periodontal disease in, 47 

Leucocytes, infiltration of tissues with, in 
papillary layer, in periodontal 
disease, 31 

Life insurance in cases of oral sepsis, 
55. 57. 58 

Lime salts, loss of, in tooth-socket, 32 

Londoners, exhumed skulls of, giving 
evidence of former good perform- 
ance of mastication, 63 

Lung symptoms and oral sepsis, connec- 
tion between, case showing, 71, 72 

— trouble developing in case of peri- 
odontal disease, 55, 57 


Macropus, skull of, showing advanced 

periodontal disease, 18 
Maltese terrier, periodontal disease in, 24 
Man, periodontal disease in, cause of, 62 

initial lesion, 53 

Mandible, bone in, skiagrams showing 

appearance of, I, 2 

Mandible from advanced case of peri- 
odontal disease in region of mandi- 
bular molars, 13, 14 

— of suricate more frequently affected 

than maxilla with periodontal 
disease, 20 

— , spread of periodontal disease greater 
in maxilla than in, 12, 13 

— , suppuration of body of, from peri- 
odontal disease, skull of deer show- 
ing, 22 

— with normal alveolar process, I, 2 
Mastication, function of, former good 

execution evidenced by condition of 

exhumed skulls of Londoners, 63 
— , well-performed, effect on alveolar 

process, 61 
or ill-performed, in relation to 

progress of periodontal disease, 61 
Maxilla showing cup-shaped absorption 

of bone round right first molar in 

periodontal disease, 8 
destruction of alveolar process in 

periodontal disease, 5, 6 
— , spread of periodontal disease greater 

in, than in mandible, 12, 13 

— with destruction of bone in chronic 

general periodontitis, 3, 4, 5 
Medalia, L. S., micro-organisms asso- 
ciated with periodontal disease, 50, 


Micrococci^ tetragenus, association with 
periodontal disease, 56 

Micro-organisms associated with peri- 
odontal disease, 49, 50, 51 

same as those responsible 

for ordinary suppuration, 51 

— in cultures from marginal gingivitis, 51 
Miller, W. D., personal experiments 

with micro-organisms in mouth, 65 
Molar, right first, cup-shaped absorption 

of bone round, in periodontal 

disease, 8 
Molars and premolars, destruction of 

bone greatest around, in chronic 

general periodontitis, 5 
— , first and second, skiagrams of, show- 
ing different degrees of destruction 

around, in periodontal disease, 8 
— , mandibular, mandible from advanced 

case of periodontal disease in region 

of, 13, 14 
— , roots of, formation of masses of 

adventitious tissue in cleft between, 15 



Monkeys, periodontal disease in, 23 

Mouth, amoeba; in, 51 / 

— , bacteriological balance in, factors 
contributing towards. 64, 65 

— , flushing with saliva, effects on micro- 
organisms, 64, 65 

— , healthy, certain organisms always 
present in, 64 

— , mucous membrane of, congestion in 
late periodontal disease, 39 

— , spirochetes in, 51 

Mouth-breathers, gingivitis in, cannot be 
removed by care and cleanliness, 57 

, liability to, 39 

, marginal, 52, 53 

, periodontal disease in, 44, 55, 59,63 

— ■ — , with periodontal disease, extrac- 
tion of teeth in, 93 

and non-mouth-breathers, starting 

point and progress of periodontal 
disease in, compared, 53 

Mouth-breathing, difficulty of over- 
coming, 77 

Muco-periosteum, normal appearance 
of, 2, 3 

— > gingival margin, 3 

Nasal breathing, promotion of, apparatus 
for, 77, 78 

, in periodontal disease, 77 

Noguchi, spirochetes of mouth, 51 

Osseous tissues, resistance of, as bar to 

progress of periodontal disease, 60 
Osteitis, rarefying, in periodontal disease, 

, absorption of toxic products 

of bacteria accompanying, 66 
, progressive in peiiodontal disease, 

, in periodontal disease, method 

of gauging, 14, 15 
Osteoid tissue, outside of tooth-socket in 

course of connection with, 34 
, transformation of tooth-socket 

into, 32, 33, 36 

Pancreatitis leading to jaundice, 70 
Pancreatic reaction (Cammidge's) in jaun- 
dice, 70 
Panolia deer ( Cervus eldii), skull showing 
periodontal disease, 20, 21 

Panolia deer (Cervus eldii), skull showing 
periodontal disease, region in which 
most marked, 20, 21 

Papilloe, interdental, congestion of, 
earliest sign of periodontal disease, 38 

, disappearance in periodontal 

disease, 43 

Payne and Eyre, micro-organisms causing 
periodontal disease, 50 

Periodontal membrane, deposit of urates 
in, 60 

Periodontitis, chronic general (peri- 
odontal disease), as active agent in 
production of pathological lesions, 64 

, clinical appearances, 38 

deceptive, 40, 41, 42, 43, 

44- 45 

--, clinical histories of cases, 55-59 

, diseases associated with, 68 

, etiology, 62 

, extent of disease revealed by 

X-rays, 42, 43, 44, 45 

, final stage, 9 

, in animals, 16 

,micro-organisms associated with, 

49. 5°- 51 

causing, 50 

, morbid anatomy of advanced 

case, 6, 7 

■ , microscopical anatomy of, 31 

, pathology, 46 

, site of origin, 4 

— ■ , spread in maxilla greater than 

in mandible, 12, 13 

, treatment, 77 

, case under, skiagrams from, 

86, 87 

, cases favourable for, 84-88 

not favourable for, 88 

, local, 78, 94 

— , gouty, so-called, 60 

Phagocytes, effect on micro-organisms of 
the mouth, 65 
,, Pharynx, mucous membrane of, conges- 
tion of, in late periodontal disease, 39 

Pierce, deposit of urates in periodontal 
membrane, 60 

Pneumococcus, frequent association with 
periodontal disease, 50, 51 

Pockets in periodontal disease, cleansing 
of, 79 

, good results from, 85 

, reduction of, by astringents, 79 

, by free removal of redun- 
dant gum, 79 



Tockets in periodontal disease, steriliza- 
tion by ionization, 101, 102 

Powell, Sir R. Douglas, cardiac irregu- 
larity ceasing on treatment of teeth, 

Piemolars and molars, destruction of 

bone greatest around, in chronic 

periodontitis, 5 
Pug-dogs (Canis familiaris), periodontal 

disease in, 24, 48 
Pyorrhoea alveolaris. See Periodontitis, 

chronic, general. 


Rheostat, use of, in electro-therapeutic 
treatment of periodontal disease, 99, 

Rheumatism, chronic and muscular, con- 
nection with periodontal disease, 72 

Royal College of Surgeons of England, 
Museum, Odontological Section, 
skulls of animals exhibiting peri- 
odontal disease, 17 

Saliva, micro-organisms conveyed from 

mouth into stomach by, 65 
Scaling, delay of, till after reduction of 

gingivitis, 78 
Sepsis, dental, chronic glossitis develop- 
ing in syphilitics with, 68 
-, oral, chronic infection of lower part 
of ileum in, 70 

, connection of gastric ulcer in old 

people with, 69 

, defined, 67 

, life insurance in cases o f , 55, 57, 58 

— — , potent source of general infection, 


and chronic gastritis, connection 

between, 68, 69 

and lung symptoms, connection 

between, 71, 72 

Skulls, exhumed, of Londoners, former 
good execution of function of masti- 
cation evidenced by condition of, 63 

Spirochuta macrodentium, 51 

— microdentium, 51 
Spirochetes in mouth, 51 
Stagnation areas about teeth of horse, 

agency in setting up periodontal 

disease, 27, 28, 46 
, cause of deposit of calculus around 

teeth, 59 
of periodontal disease, 77 

Stagnation areas, material collecting in, 

forming toxins, 53 
Sternberg, early observation of amcebre 

about teeth, 51 
Stomach, conveyance of niicro-organi>ms 

from mouth into, 64, 65 
— , fate of micro-organisms fiom mouth 

reaching, 65 
— , ulcer of, in old people, connection 

with oral sepsis, 69 
Streptococci, overwhelming prepon- 
derance in mouth. 64 
Suricate [Suricata letradaclyld) mandible 

showing periodontal disease, 19, 20 
Syphilitics with dental sepsis, chronic 

glossitis developing in, 68 

Tannic acid in reduction of pockets, 79 

, indelible stain left by, 79 

Teeth, anterior aspects of, destruction of 

bone most marked on, case showing 

11, 12 

— — , retention of, in periodontal 

disease when permissible, 93 
— , brittleness of, in periodontal disease, 

presumed cause of, 15 
— , deposit of calculus around, cause of, 


— exhibiting deep pockets and profuse 

suppuration in periodontal disease, 
14, 15 
— , extraction of, curing "chronic ill- 
health," 71 

— — , in periodontal disease, 55, 56, 59 

, good results from, 89 

, in case of mouth-breathers, 93 

in cases having causal rela- 
tionship to other diseases, 92 

■ , method, 92 

, opposition to, 94 

, reasons for, 89, 90, 94 

— falling out in final stage of periodontal 

disease, 9 

— from case of periodontal disease asso- 

ciated with multiple arthritis, 14, 15 

— from cases of periodontal disease 

showing translucent areas, 16 
— , functional activity of, growth of sur- 
rounding bone tissues dependent on, 

, rarely brought into play by 

articles of modern diet, 61 
— , pockets around , in periodontal disease, 
38, 39 



Teeth showing changes at apices in peri- 
odontal disease, 15 

Thomson, J. G. and D., association of 
spirochetes with severe pyorrhoea, 

Tissue reaction against spread of peri- 
odontal disease, 53, 54 
in periodontal disease, failure of, 


Tonsils, congestion of, in advanced 
periodontal disease, 39 

Tooth-socket, bone of, lacunar absorp- 
tion, so-called, 37 

, main features of changes in ad- 
vanced periodontal disease, 36, 37 

, marrow part, concluding stages 

of development of periodontal 
disease in, 35, 37 

, primary alterations in peri- 
odontal disease, 35, 37 

— , in cats, destruction of tissues forming, 


— , loss of lime salts, 32 

— , outside of, in course of connection 
with osteoid tissue, 34 

— , transformation into fibrous connec- 
tive tissue, 32-37 

into osteoid tissue, 32, 33, 36 

Toxremia, chronic, a form of chronic ill- 
health, 71 

— , intestinal, process of, described, 66 

Toxic products of bacteria, absorption 
into general circulation in peri- 
odontal disease, 66, 67 

of alimentary canal, fate of, 66 

Toxins in periodontal disease, formation 
from material collectingin stagnation 
areas, 53 

, passage into general circulation, 



URATES, deposit in periodontal mem- 
brane, 60 

VACCINE therapy in periodontal disease, 

81, 85, 95 

, causes of failure, 95 

complicated by iritis, case of, 

reason for success, 96, 97 
, " cured " cases probably only 

relieved, 96 

, dosage, 82 

, method of obtaining cultures 

for vaccines from patient, 81 
Vaccines, preparation of, 82 


Wallaby, Bennett's [Macropus bennetti), 

skull showing early periodontal 

disease, 17 
Wild animals living in captivity, cause of 

periodontal disease among, 48 
, fed on fresh meat, almost 

entirely free from periodontal 

disease, 48 

, periodontal disease in, 17, 48 

, common among those living 

in captivity, 48 
, rare among those living in 

wild state, 48 
Wolf, common (Canis lupus), skull of, 

showing periodontal disease, 19 
Woodruff, IL, method for producing 

hyperemia of gums, 83 


X-RAY examination in periodontal 

disease, 40, 41, 42, 43 
, must supplement clinical 

examination, 40 

ZlNC chloride, valuable in electrical 
treatment of periodontal disease, 99 

Znamensky, microscopical anatomy of 
periodontal disease, 31